ucp2 Search Results


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  • 98
    Thermo Fisher gene exp ucp2 rn01754856 m1
    Resveratrol pretreatment decreases <t>UCP2</t> levels after 48 hours in mitochondria isolated from rat hippocampus
    Gene Exp Ucp2 Rn01754856 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 98/100, based on 77 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Millipore rabbit anti ucp2
    Genipin upregulates <t>UCP2</t> and FAT/CD36. ( A ) Western blot analysis of UCP2 and FAT/CD36 expressions. The protein was isolated from the HepG2 cells after 24 h of exposure to control medium, palmitic acid (PA, 250 μmol/L) and PA plus genipin (5 μmol/L). Equal protein loading was confirmed using β-actin antibody. ( B ) Target proteins/β-actin is shown in the bar graph. ** p
    Rabbit Anti Ucp2, supplied by Millipore, used in various techniques. Bioz Stars score: 93/100, based on 26 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Santa Cruz Biotechnology ucp2
    Role of <t>UCP2</t> in Wy-14,643 protection against APAP-induced liver toxicity using Ucp2 -null mice. (A) QPCR analysis of UCP2 mRNA in livers from control, Wy-14,643-treated, APAP-treated, and Wy-14,643/APAP treated wild-type mice. (B) Serum ALT and AST enzyme levels from control, Wy-14,643-treated, APAP-treated, and Wy-14,643/APAP-treated Ucp2 -null mice. (C) H E staining of livers from Wy-14,643-treated, APAP-treated, and Wy-14,643/APAP-treated Ucp2 -null mice. **p
    Ucp2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 435 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ucp2  (Abcam)
    93
    Abcam ucp2
    mRNA expression levels and protein levels of Trpv1 and <t>Ucp2</t> in liver of control (C), western diet (WD), hesperidin (HESP), capsaicin (CAP), and hesperidin and capsaicin (HESP + CAP) rats at the end of treatment. mRNA levels were measured by real-time PCR. Specific protein levels were measured by western blot. Representative bands for TRPV1 and UCP2 (deriving for each protein from the same gel), together with β-actin are shown. mRNA and protein levels were expressed as a percentage of the control group. Data are mean ± SEM (n = 7–8). Statistical analysis between groups was performed by one-way ANOVA, followed by LSD post-hoc analysis ( P
    Ucp2, supplied by Abcam, used in various techniques. Bioz Stars score: 93/100, based on 232 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Cell Signaling Technology Inc ucp2
    Hydrogen peroxide was critical for PLCγ-1 activation in <t>UCP2</t> overexpressed cells Removal of hydrogen peroxide by catalase ( A ) suppressed lipid peroxidation ( B , N=4 per group), PLCγ-1 induction ( C , Fra-I is a subunit of the activator protein 1, which is activated during skin carcinogenesis) and the levels of its downstream targets: IP3 ( D , N=3 per group) and DAG ( E , N=3 per group), as well as 3D spheroid formation ( F , N=6 per group) of UCP2 overexpressed cells. *, p
    Ucp2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 91/100, based on 112 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Shanghai GenePharma ucp2
    The transfection and knockdown efficiency of siRNA against <t>UCP2</t> in H9C2 cells. (A and B) H9C2 cells transfected with control siRNA (Cy3) emitted red fluorescence. The transfection efficiency is expressed as the ratio of the number of red fluorescence cells over all cells by fluorescence microscopy (magnification, x20). (C) The knockdown efficiency of siRNA against UCP2 in H9C2 cells. H9C2 cells were left untransfected (control), transfected with Lipofectamine 2000 (no siRNA), transfected with negative control siRNA (ncRNA), or transfected with siRNA1 or 2. After 24 h, the mRNA levels of uncoupling protein 2 (UCP2) were determined by RT-qPCR with normalization to 18s RNA. * P
    Ucp2, supplied by Shanghai GenePharma, used in various techniques. Bioz Stars score: 93/100, based on 432 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Alpha Diagnostics ucp 2
    Effect of <t>UCP-2</t> knockdown on Bcl-2 expression and cyanide toxicity. Cells were transfected with UCP-2 RNAi and 24 h later treated with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 12 h. (A) Bcl-2 levels as detected by Western
    Ucp 2, supplied by Alpha Diagnostics, used in various techniques. Bioz Stars score: 90/100, based on 71 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Santa Cruz Biotechnology anti ucp2
    Pretreatment with EPA or DHA prevents the doxorubicin-induced decrease in <t>UCP2</t> protein expression. H9C2 cells were left untreated or were treated with 50 μM DHA or 100 μM EPA for 24 h, then were left untreated or wre treated with 1 μM doxorubicin (DOX) in the continued presence of the fatty acid for 24 h. After treatment, the cells were harvested and proteins extracted for Western blotting using antibody against UCP2 with ß-actin as the internal control. The bars are the quantitative density analysis expressed as the relative density compared to that in the untreated control and are the mean ± S.D. for three separate experiments. **, ***: p
    Anti Ucp2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 88/100, based on 67 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    OriGene ucp2
    Mutant p53 inhibits <t>UCP2</t> and PGC-1α through the inhibition of SESN1/AMPK signaling. a MDA-MB-231 cells were transduced with lentiviruses containing p53-SH1 or p53-SH2 vectors for mutant p53 silencing or their non-targeting negative control (NT). Left panel: western blotting was performed using 50 μg of whole-protein extracts and probed with the indicated antibodies. The p53 expression was shown as control of p53 knockdown efficacy and the GAPDH expression was used as control of equal proteins loading. Right panel: AMPK was immunoprecipitated from protein extracts using anti-rabbit AMPK antibody (IP: AMPK) and western blot analysis was performed using indicated antibodies. Protein extracts from cells silenced for p53 expression with p53-SH1 or p53-SH2 vectors were also immunoprecipitated with rabbit IgG as control. The blot exhibits equivalent AMPK levels in all samples. b H1299 p53-null cells stably expressing R273H mutant p53 (clone H1) and its respective mock control (clone C9) were used to confirm the regulation of SESN1:AMPK by mutant p53. Left panel: western blotting was performed using 50 μg of whole-protein extracts and probed with the indicated antibodies. Right panel: SESN1 was immunoprecipitated from protein extracts using anti-SESN1 antibody (IP: SESN1) and western blot analysis was performed using indicated antibodies. Protein extracts were also immunoprecipitated with IgG as con trol. c AsPC1-p53 null cells were transfected with the vectors for the ectopic expression of p53-R273H and its mock control and treated with 1 mM AICA-R for 48 h. Gene expression analysis of the UCP2 and PGC-1α was performed by RT-qPCR and normalized to GAPDH mRNA. # p
    Ucp2, supplied by OriGene, used in various techniques. Bioz Stars score: 92/100, based on 46 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Millipore ucp2
    Wld S downregulates <t>UCP2</t> expression and upregulates ATP levels through SIRT1. A : Wld S colocalized with SIRT1 in MIN6 cells. The stable cell lines expressing EGFP-Wld S were transiently transfected with pCMV-myc-SIRT1 and stained with anti-Myc antibody and DAPI. Scale bar, 5 μm. B : Wld S was coimmunoprecipitated with SIRT1 from the pancreatic lysates of Wld S mice. C : Wld S and its enzyme-dead mutant Wld S -H112A coimmunoprecipitated with SIRT1. The MIN6 cells stably expressing EGFP, EGFP-Wld S , or EGFP-Wld S -H112A were used for immunoprecipitation. UCP2 protein levels were also detected by Western blot. D and E : Liquid chromatography-tandem mass spectrometry analysis of NMN, NADP, NADPH, NAD, NADH, NA, and NAM extracted from pancreas of 9-week-old wild-type (WT) ( D ) or Wld S mice ( E ). *With significant difference. F : Quantification of the small molecules corresponding to D and E showed that NAD and NMN levels were upregulated in the pancreas of Wld S mice ( n = 4 for each genotype). G : Wld S repressed UCP2 promoter activity like SIRT1. UCP2 promoter activity was measured by luciferase assay in 293T cells transfected with pGL3-UCP2-Promoter and the indicated plasmids. H : Wld S downregulated UCP2 mRNA levels dependent on its enzyme activity. UCP2 mRNA level was measured by real-time PCR with MIN6 cell lines stably expressing EGFP, EGFP-Wld S , and EGFP-Wld S -H112A. I : Wld S downregulated UCP2 mRNA levels via SIRT1. UCP2 mRNA levels were determined by real-time PCR using islets isolated from mice with the indicated genotype ( n = 4 for each genotype). J : Wld S downregulated UCP2 protein levels via SIRT1. The protein levels in brown fat tissue with the indicated genotype were detected with SIRT1, Wld S , UCP2, and tubulin antibodies ( n = 3 for each genotype). K : Quantification of the UCP2 protein levels corresponding to J . L : Wld S increased ATP levels in primary cultured islets at the indicated glucose concentration ( n = 3). M : Wld S upregulated ATP level in islets via SIRT1. ATP levels were measured in islets with indicated genotypes at 2 mmol/L or 20 mmol/L glucose ( n = 3). * P
    Ucp2, supplied by Millipore, used in various techniques. Bioz Stars score: 88/100, based on 75 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    95
    Abcam anti ucp2
    DCA increases mitochondrial OXPHOS and ROS production in A2780 cells compared with A2780/DDP cells. Notes: Mitochondrial citrate ( A ) and the OCR ( B ) were measured in the presence of DCA at the indicated doses for 24 hours. Mitochondrial ROS ( C ) and overall ROS ( E ) were detected in A2780 and A2780/DDP cells treated with DCA at the indicated doses for 24 hours by measuring fluorescence intensities using fluorescence microscopy (×200) or flow cytometry, respectively. ( D ) Expression levels of <t>UCP2</t> protein in A2780 and A2780/DDP cells after DCA treatment. Data are presented as mean ± SE, n=3. * P
    Anti Ucp2, supplied by Abcam, used in various techniques. Bioz Stars score: 95/100, based on 56 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ucp 2  (EIAab)
    90
    EIAab ucp 2
    DCA increases mitochondrial OXPHOS and ROS production in A2780 cells compared with A2780/DDP cells. Notes: Mitochondrial citrate ( A ) and the OCR ( B ) were measured in the presence of DCA at the indicated doses for 24 hours. Mitochondrial ROS ( C ) and overall ROS ( E ) were detected in A2780 and A2780/DDP cells treated with DCA at the indicated doses for 24 hours by measuring fluorescence intensities using fluorescence microscopy (×200) or flow cytometry, respectively. ( D ) Expression levels of <t>UCP2</t> protein in A2780 and A2780/DDP cells after DCA treatment. Data are presented as mean ± SE, n=3. * P
    Ucp 2, supplied by EIAab, used in various techniques. Bioz Stars score: 90/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    98
    Thermo Fisher gene exp ucp2 mm00627599 m1
    High-Fat Diet Induces a Rapid and Transient Upregulation of <t>Ucp2</t> mRNA Levels and a Rapid and Transient Change in Mitochondrial Morphology A–E) Real-time PCR data showing relative mRNA levels of Ucp2 (A), IL-1β (B), IL-6 (C), Tnfα (D), and Cx3cr1 (E) in isolated hypothalamic microglia (CD11b + cells) from male mice fed on standard chow diet (SD), 3-day high-fat diet (3d HFD), 7-day HFD (7d HFD), or 8-week HFD (8w HFD) (n = 4–6 mice per group). (F) Representative electron micrographs showing mitochondria (asterisks) in microglial cells in the arcuate nucleus of the hypothalamus of male mice exposed to SD, 3d HFD, 7d HFD, or 8w HFD. (G–I) Average mitochondrial area (G), mitochondrial density (H), and mitochondrial coverage (I), in microglial cells from male mice fed on SD (n = 5), 3d HFD (n = 6), 7d HFD (n = 5), or 8w HFD (n = 5). (J) Graph showing the percentage of phosphorylated DRP1 (p-Drp1) at site S616 (activated form) in tomato-positive cells (microglia) in the hypothalamus and cortex of mice exposed to either standard chow diet (SD; n = 3) or 3d HFD (n = 5). .
    Gene Exp Ucp2 Mm00627599 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 98/100, based on 34 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Thermo Fisher gene exp ucp2 hs01075227 m1
    Effects of 100 μM 1-monooleyl glycerol (1-MOG) and 2-monooley glycerol (2-MOG) on expression of mRNA of acyl-CoA oxidase (ACO)  A ) medium-chain acyl-CoA dehydrogenase (MCAD)  B ) fatty acid translocase (FAT)  C ) and uncoupling protein-2 (UCP-2)  D ) in the Caco-2 cells. Notes:  Boxes and bars indicate mean ± SD of relative quantitation mRNA values using 18S as an internal control. N = 8. * P
    Gene Exp Ucp2 Hs01075227 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 85/100, based on 20 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    98
    Thermo Fisher gene exp ucp2 mm00627598 m1
    The relative gene expression of SREBP1 ( Srebf1 ), PPAR‐alpha ( Ppara ), DGAT‐1 ( Dgat1 ), FAS ( Fasn ) and ACC1 ( Acaca ) in the liver (A) and SREBP1 ( Srebf1 ), PPAR‐alpha ( Ppara ), DGAT‐1 ( Dgat1 ), <t>UCP2</t> ( Ucp2 ) and HSL ( Lipe ) in the adipose tissue (B) with regard to SKL‐14959 treatment. Values are expressed as means ± standard deviation (eight to nine mice per group). # p
    Gene Exp Ucp2 Mm00627598 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 98/100, based on 107 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Santa Cruz Biotechnology goat anti ucp2
    <t>UCP2</t> decreases mast cell histidine decarboxylase expression
    Goat Anti Ucp2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 88/100, based on 44 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    89
    Thermo Fisher gene exp ucp2 hs00163349 m1
    A set of ROS regulating enzymes is coordinately controlled by PPARγ activation. Karpas 299 and SUP-M2 cells treated with 2 μmol/L rosiglitazone or DMSO were harvested at 42 hours after serum withdrawal. A: p67 mRNA was measured by real-time RT-PCR (left). The amount of p67 mRNA in DMSO-treated Karpas 299 cells was arbitrarily set as 100%. p67 protein levels were determined by Western blot analysis in whole-cell lysates (right). D, DMSO; R, rosiglitazone. B: <t>UCP2</t> mRNA was measured by real-time RT-PCR (left). The amount of UCP2 mRNA in DMSO-treated Karpas 299 cells was arbitrarily set as 100%. UCP2 protein levels were determined by Western blot analysis in whole cell lysates (right). D, DMSO; R, rosiglitazone. C: Mn-SOD mRNA was measured by real-time RT-PCR (left). The amount of Mn-SOD mRNA in DMSO-treated Karpas 299 cells was arbitrarily set as 100%. Mn-SOD activity was determined in whole-cell lysates. D: CuZn-SOD and catalase mRNA levels were determined by real-time RT-PCR. The amount of mRNA in DMSO-treated Karpas 299 cells was arbitrarily set as 100%. Data shown in A–D are mean ± SE of at least three independent experiments.
    Gene Exp Ucp2 Hs00163349 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 89/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    87
    Thermo Fisher gene exp ucp2 mm00627597 m1
    AMPK activation does not cause a miR-122 down-regulation. A , Mice were treated with metformin (250 mg/kg, ip. ) twice a day at a 12 h-interval for 3 days or 5 days and were sacrificed 12 h after the final treatment. Activated and total AMPK levels in the liver of mice were determined by Western blot analysis using anti-phospho-AMPKα (Thr 172) and AMPKα specific antibodies, respectively (the top panel). Levels of phospho-AMPKα was normalized with respective AMPKα and are illustrated as the % of control group (the second panel). <t>UCP2</t> mRNA (the third panel) and miR-122 (the last panel) levels were determined by the quantitative RT-PCR, were normalized with β-actin and the U6 snRNA, respectively, and are illustrated as the % of control group. *, p
    Gene Exp Ucp2 Mm00627597 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 87/100, based on 20 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Resveratrol pretreatment decreases UCP2 levels after 48 hours in mitochondria isolated from rat hippocampus

    Journal: Neuroscience

    Article Title: RESVERATROL PRETREATMENT PROTECTS RAT BRAIN FROM CEREBRAL ISCHEMIC DAMAGE VIA A SIRT1 – UCP2 PATHWAY

    doi: 10.1016/j.neuroscience.2009.01.017

    Figure Lengend Snippet: Resveratrol pretreatment decreases UCP2 levels after 48 hours in mitochondria isolated from rat hippocampus

    Article Snippet: The following gene-specific probe/primer pair mixtures were used: β-actin (Rm00667869_m1) and UCP2 (Rn01754856_m1).

    Techniques: Isolation

    Genipin upregulates UCP2 and FAT/CD36. ( A ) Western blot analysis of UCP2 and FAT/CD36 expressions. The protein was isolated from the HepG2 cells after 24 h of exposure to control medium, palmitic acid (PA, 250 μmol/L) and PA plus genipin (5 μmol/L). Equal protein loading was confirmed using β-actin antibody. ( B ) Target proteins/β-actin is shown in the bar graph. ** p

    Journal: Lipids in Health and Disease

    Article Title: Inhibition of uncoupling protein 2 with genipin exacerbates palmitate-induced hepatic steatosis

    doi: 10.1186/1476-511X-11-154

    Figure Lengend Snippet: Genipin upregulates UCP2 and FAT/CD36. ( A ) Western blot analysis of UCP2 and FAT/CD36 expressions. The protein was isolated from the HepG2 cells after 24 h of exposure to control medium, palmitic acid (PA, 250 μmol/L) and PA plus genipin (5 μmol/L). Equal protein loading was confirmed using β-actin antibody. ( B ) Target proteins/β-actin is shown in the bar graph. ** p

    Article Snippet: Lysate was electrophoretically transferred onto a nitrocellulose membrane and immunoblotted with rabbit anti-UCP2 and FAT/CD36 IgG (1:500 dilution, Sigma-Aldrich Co., USA).

    Techniques: Western Blot, Isolation

    Role of UCP2 in Wy-14,643 protection against APAP-induced liver toxicity using Ucp2 -null mice. (A) QPCR analysis of UCP2 mRNA in livers from control, Wy-14,643-treated, APAP-treated, and Wy-14,643/APAP treated wild-type mice. (B) Serum ALT and AST enzyme levels from control, Wy-14,643-treated, APAP-treated, and Wy-14,643/APAP-treated Ucp2 -null mice. (C) H E staining of livers from Wy-14,643-treated, APAP-treated, and Wy-14,643/APAP-treated Ucp2 -null mice. **p

    Journal: Hepatology (Baltimore, Md.)

    Article Title: PPAR?-dependent Induction of Uncoupling Protein 2 Protects Against Acetaminophen-Induced Liver Toxicity

    doi: 10.1002/hep.25645

    Figure Lengend Snippet: Role of UCP2 in Wy-14,643 protection against APAP-induced liver toxicity using Ucp2 -null mice. (A) QPCR analysis of UCP2 mRNA in livers from control, Wy-14,643-treated, APAP-treated, and Wy-14,643/APAP treated wild-type mice. (B) Serum ALT and AST enzyme levels from control, Wy-14,643-treated, APAP-treated, and Wy-14,643/APAP-treated Ucp2 -null mice. (C) H E staining of livers from Wy-14,643-treated, APAP-treated, and Wy-14,643/APAP-treated Ucp2 -null mice. **p

    Article Snippet: The present study demonstrates a novel, protective role for PPARα during APAP-induced hepatotoxicity and sheds mechanistic insight into the importance of UCP2 in mediating these protective effects.

    Techniques: Mouse Assay, Real-time Polymerase Chain Reaction, AST Assay, Staining

    Role of UCP2 in Wy-14,643 protection against APAP-induced liver toxicity using forced expression of UCP2 in livers of wild-type mice. (A) Effect of Ad- Ucp2 and Ad- Cre prior to APAP treatment on serum ALT and AST enzyme levels. (B) Effect of Ad- Ucp2 and Ad- Cre prior to APAP treatment on total mitochondrial GSH levels in livers of wild-type mice. (C) Effect of Ad- Ucp2 and Ad- Cre prior to APAP treatment on JNK and p-JNK protein levels in livers of wild-type mice. (D) ALT enzyme levels in APAP and Ad- Ucp2 treated mice after 24 h APAP treatment. *p

    Journal: Hepatology (Baltimore, Md.)

    Article Title: PPAR?-dependent Induction of Uncoupling Protein 2 Protects Against Acetaminophen-Induced Liver Toxicity

    doi: 10.1002/hep.25645

    Figure Lengend Snippet: Role of UCP2 in Wy-14,643 protection against APAP-induced liver toxicity using forced expression of UCP2 in livers of wild-type mice. (A) Effect of Ad- Ucp2 and Ad- Cre prior to APAP treatment on serum ALT and AST enzyme levels. (B) Effect of Ad- Ucp2 and Ad- Cre prior to APAP treatment on total mitochondrial GSH levels in livers of wild-type mice. (C) Effect of Ad- Ucp2 and Ad- Cre prior to APAP treatment on JNK and p-JNK protein levels in livers of wild-type mice. (D) ALT enzyme levels in APAP and Ad- Ucp2 treated mice after 24 h APAP treatment. *p

    Article Snippet: The present study demonstrates a novel, protective role for PPARα during APAP-induced hepatotoxicity and sheds mechanistic insight into the importance of UCP2 in mediating these protective effects.

    Techniques: Expressing, Mouse Assay, AST Assay

    Role of UCP2 in Wy-14,643 protection against APAP-induced liver toxicity using forced expression of UCP2 in livers of wild-type mice. H E staining of livers from wild-type mice administered Ad- Ucp2 and Ad- Cre prior to APAP treatment. Western blot of UCP2 protein in Ad- Ucp2 and Ad- Cre treated mice. Uptake of virus was monitored by PCR of Cre recombinase cDNA.

    Journal: Hepatology (Baltimore, Md.)

    Article Title: PPAR?-dependent Induction of Uncoupling Protein 2 Protects Against Acetaminophen-Induced Liver Toxicity

    doi: 10.1002/hep.25645

    Figure Lengend Snippet: Role of UCP2 in Wy-14,643 protection against APAP-induced liver toxicity using forced expression of UCP2 in livers of wild-type mice. H E staining of livers from wild-type mice administered Ad- Ucp2 and Ad- Cre prior to APAP treatment. Western blot of UCP2 protein in Ad- Ucp2 and Ad- Cre treated mice. Uptake of virus was monitored by PCR of Cre recombinase cDNA.

    Article Snippet: The present study demonstrates a novel, protective role for PPARα during APAP-induced hepatotoxicity and sheds mechanistic insight into the importance of UCP2 in mediating these protective effects.

    Techniques: Expressing, Mouse Assay, Staining, Western Blot, Polymerase Chain Reaction

    Role of UCP2 in Wy-14,643 protection against APAP-induced liver toxicity using Ucp2 -null mice. (A) QPCR analysis of MCAD, CPT1, and PDK4 mRNA in livers from control, Wy-14,643-treated, APAP-treated, and Wy-14,643/APAP-treated Ucp2 -null mice. (B) Levels of mitochondrial GSH control, Wy-14,643-treated, APAP-treated, and Wy-14,643/APAP-treated Ucp2 -null mice. (C) Levels of p-JNK, JNK, and p-c-jun proteins in livers from control, Wy-14,643-treated, APAP-treated, and Wy-14,643/APAP-treated Ucp2 -null mice. *p

    Journal: Hepatology (Baltimore, Md.)

    Article Title: PPAR?-dependent Induction of Uncoupling Protein 2 Protects Against Acetaminophen-Induced Liver Toxicity

    doi: 10.1002/hep.25645

    Figure Lengend Snippet: Role of UCP2 in Wy-14,643 protection against APAP-induced liver toxicity using Ucp2 -null mice. (A) QPCR analysis of MCAD, CPT1, and PDK4 mRNA in livers from control, Wy-14,643-treated, APAP-treated, and Wy-14,643/APAP-treated Ucp2 -null mice. (B) Levels of mitochondrial GSH control, Wy-14,643-treated, APAP-treated, and Wy-14,643/APAP-treated Ucp2 -null mice. (C) Levels of p-JNK, JNK, and p-c-jun proteins in livers from control, Wy-14,643-treated, APAP-treated, and Wy-14,643/APAP-treated Ucp2 -null mice. *p

    Article Snippet: The present study demonstrates a novel, protective role for PPARα during APAP-induced hepatotoxicity and sheds mechanistic insight into the importance of UCP2 in mediating these protective effects.

    Techniques: Mouse Assay, Real-time Polymerase Chain Reaction

    The redox state from isolated mitochondria was compared in WT mice with and without pioglitazone (Pio) and UCP-2 KO mouse hearts and demonstrated no differences under basal conditions between reduced (GSH) and total glutathione (GSH + GSSG) concentrations. GSH/GSSG in mitochondria from WT mice on regular and pioglitazone diets were 7.7±3.6 and 12.5±7.3 respectively and did not differ from UCP-2 KO mice with either diet (NS). Data are expressed as means and SEM.

    Journal: Translational Research

    Article Title: Uncoupling Protein-2 Expression and Effects on Mitochondrial Membrane Potential and Oxidant Stress in Heart Tissue

    doi: 10.1016/j.trsl.2011.11.001

    Figure Lengend Snippet: The redox state from isolated mitochondria was compared in WT mice with and without pioglitazone (Pio) and UCP-2 KO mouse hearts and demonstrated no differences under basal conditions between reduced (GSH) and total glutathione (GSH + GSSG) concentrations. GSH/GSSG in mitochondria from WT mice on regular and pioglitazone diets were 7.7±3.6 and 12.5±7.3 respectively and did not differ from UCP-2 KO mice with either diet (NS). Data are expressed as means and SEM.

    Article Snippet: There are several experimental observations in various animal models that also suggest that UCP-2 plays an important role as an antioxidant.

    Techniques: Isolation, Mouse Assay

    The relationship between state 2 respiration and inner membrane potential is shown in isolated mitochondria from heart tissue extracted from UCP-2 KO mice and WT mice with or without chronic PPARγ stimulation with dietary supplementation of pioglitazone. The presence of a proton leak across the inner membrane induced by UCP-2 is associated with a higher state 2 respiration relative to the lower membrane potential, in mice with increased expression of UCP-2. Data are expressed as means and SEM bars.

    Journal: Translational Research

    Article Title: Uncoupling Protein-2 Expression and Effects on Mitochondrial Membrane Potential and Oxidant Stress in Heart Tissue

    doi: 10.1016/j.trsl.2011.11.001

    Figure Lengend Snippet: The relationship between state 2 respiration and inner membrane potential is shown in isolated mitochondria from heart tissue extracted from UCP-2 KO mice and WT mice with or without chronic PPARγ stimulation with dietary supplementation of pioglitazone. The presence of a proton leak across the inner membrane induced by UCP-2 is associated with a higher state 2 respiration relative to the lower membrane potential, in mice with increased expression of UCP-2. Data are expressed as means and SEM bars.

    Article Snippet: There are several experimental observations in various animal models that also suggest that UCP-2 plays an important role as an antioxidant.

    Techniques: Isolation, Mouse Assay, Expressing

    The relationship between maximal superoxide levels during inhibition of complex III with antimycin A and inner membrane potential is shown in isolated mitochondria from heart tissue extracted from UCP-2 KO mice and WT mice with or without pioglitazone. The presence of a proton leak across the inner membrane induced by over-expression of UCP-2 is associated with lower levels of superoxide, in mice with increased expression of UCP-2. Data are expressed as means and SEM bars.

    Journal: Translational Research

    Article Title: Uncoupling Protein-2 Expression and Effects on Mitochondrial Membrane Potential and Oxidant Stress in Heart Tissue

    doi: 10.1016/j.trsl.2011.11.001

    Figure Lengend Snippet: The relationship between maximal superoxide levels during inhibition of complex III with antimycin A and inner membrane potential is shown in isolated mitochondria from heart tissue extracted from UCP-2 KO mice and WT mice with or without pioglitazone. The presence of a proton leak across the inner membrane induced by over-expression of UCP-2 is associated with lower levels of superoxide, in mice with increased expression of UCP-2. Data are expressed as means and SEM bars.

    Article Snippet: There are several experimental observations in various animal models that also suggest that UCP-2 plays an important role as an antioxidant.

    Techniques: Inhibition, Isolation, Mouse Assay, Over Expression, Expressing

    In isolated mitochondria exposed to 10 minutes anoxia-reoxygenation, (A) state 3 respiration and (B) the respiratory control index (RCI) were higher in hearts extracted from WT mice on control (C) and Pioglitazone (Pio) diet compared with UCP-2 KO mice on either C or Pio (*P

    Journal: Translational Research

    Article Title: Uncoupling Protein-2 Expression and Effects on Mitochondrial Membrane Potential and Oxidant Stress in Heart Tissue

    doi: 10.1016/j.trsl.2011.11.001

    Figure Lengend Snippet: In isolated mitochondria exposed to 10 minutes anoxia-reoxygenation, (A) state 3 respiration and (B) the respiratory control index (RCI) were higher in hearts extracted from WT mice on control (C) and Pioglitazone (Pio) diet compared with UCP-2 KO mice on either C or Pio (*P

    Article Snippet: There are several experimental observations in various animal models that also suggest that UCP-2 plays an important role as an antioxidant.

    Techniques: Isolation, Mouse Assay

    Chronic peroxisome proliferator-activator receptor γ (PPARγ) stimulation was provided with daily pioglitazone (Pio) in the diet for 3 weeks of wild type (WT) and uncoupling protein (UCP)-2 knock-out (KO) mice. Pioglitazone increased (A) UCP-2 content in mitochondria from excised hearts of wild type mice, with no expression noted in UCP-2 KO mice and (B) PGC1-α in the nuclear fraction of WT mice.

    Journal: Translational Research

    Article Title: Uncoupling Protein-2 Expression and Effects on Mitochondrial Membrane Potential and Oxidant Stress in Heart Tissue

    doi: 10.1016/j.trsl.2011.11.001

    Figure Lengend Snippet: Chronic peroxisome proliferator-activator receptor γ (PPARγ) stimulation was provided with daily pioglitazone (Pio) in the diet for 3 weeks of wild type (WT) and uncoupling protein (UCP)-2 knock-out (KO) mice. Pioglitazone increased (A) UCP-2 content in mitochondria from excised hearts of wild type mice, with no expression noted in UCP-2 KO mice and (B) PGC1-α in the nuclear fraction of WT mice.

    Article Snippet: There are several experimental observations in various animal models that also suggest that UCP-2 plays an important role as an antioxidant.

    Techniques: Knock-Out, Mouse Assay, Expressing

    mRNA expression levels and protein levels of Trpv1 and Ucp2 in liver of control (C), western diet (WD), hesperidin (HESP), capsaicin (CAP), and hesperidin and capsaicin (HESP + CAP) rats at the end of treatment. mRNA levels were measured by real-time PCR. Specific protein levels were measured by western blot. Representative bands for TRPV1 and UCP2 (deriving for each protein from the same gel), together with β-actin are shown. mRNA and protein levels were expressed as a percentage of the control group. Data are mean ± SEM (n = 7–8). Statistical analysis between groups was performed by one-way ANOVA, followed by LSD post-hoc analysis ( P

    Journal: Scientific Reports

    Article Title: Hesperidin and capsaicin, but not the combination, prevent hepatic steatosis and other metabolic syndrome-related alterations in western diet-fed rats

    doi: 10.1038/s41598-018-32875-4

    Figure Lengend Snippet: mRNA expression levels and protein levels of Trpv1 and Ucp2 in liver of control (C), western diet (WD), hesperidin (HESP), capsaicin (CAP), and hesperidin and capsaicin (HESP + CAP) rats at the end of treatment. mRNA levels were measured by real-time PCR. Specific protein levels were measured by western blot. Representative bands for TRPV1 and UCP2 (deriving for each protein from the same gel), together with β-actin are shown. mRNA and protein levels were expressed as a percentage of the control group. Data are mean ± SEM (n = 7–8). Statistical analysis between groups was performed by one-way ANOVA, followed by LSD post-hoc analysis ( P

    Article Snippet: RNA purification system, and mRNA levels of Trpv1 and Ucp2 were measured as previously described .

    Techniques: Expressing, Western Blot, Real-time Polymerase Chain Reaction

    mRNA levels of Trpv1 and Ucp2 in HepG2 cells treated with hesperidin (HESP) (5 μmol/L and 10 μmol/L), capsaicin (CAP) (0.5 μmol/L and 1 μmol/L), the combination of both HESP + CAP, or the vehicle for 24 hours. mRNA levels were measured by real-time PCR and expressed as a percentage of the vehicle group. Data are mean ± SEM (n = 7–12). Non significant differences were found between groups by one-way ANOVA, followed by LSD post-hoc analysis (P

    Journal: Scientific Reports

    Article Title: Hesperidin and capsaicin, but not the combination, prevent hepatic steatosis and other metabolic syndrome-related alterations in western diet-fed rats

    doi: 10.1038/s41598-018-32875-4

    Figure Lengend Snippet: mRNA levels of Trpv1 and Ucp2 in HepG2 cells treated with hesperidin (HESP) (5 μmol/L and 10 μmol/L), capsaicin (CAP) (0.5 μmol/L and 1 μmol/L), the combination of both HESP + CAP, or the vehicle for 24 hours. mRNA levels were measured by real-time PCR and expressed as a percentage of the vehicle group. Data are mean ± SEM (n = 7–12). Non significant differences were found between groups by one-way ANOVA, followed by LSD post-hoc analysis (P

    Article Snippet: RNA purification system, and mRNA levels of Trpv1 and Ucp2 were measured as previously described .

    Techniques: Real-time Polymerase Chain Reaction

    Gene expression in hepatic tissues in the different groups. The mRNA and protein expression levels in hepatic tissues in the HF and three PSEs intervention groups were compared with those in the NC group. The PSEs treatments at the three doses resulted in significant down-regulation of TGF-β1, TGF-β2, TNF-α, and UCP-2 expression and slight up-regulation of ELOVL-2 expression. The effects of PSEs on PPAR-α, PPAR-γ and LXR-α expression differed. The data are expressed as the mean ± standard deviation. Δ P

    Journal: Scientific Reports

    Article Title: Phytosterol esters attenuate hepatic steatosis in rats with non-alcoholic fatty liver disease rats fed a high-fat diet

    doi: 10.1038/srep41604

    Figure Lengend Snippet: Gene expression in hepatic tissues in the different groups. The mRNA and protein expression levels in hepatic tissues in the HF and three PSEs intervention groups were compared with those in the NC group. The PSEs treatments at the three doses resulted in significant down-regulation of TGF-β1, TGF-β2, TNF-α, and UCP-2 expression and slight up-regulation of ELOVL-2 expression. The effects of PSEs on PPAR-α, PPAR-γ and LXR-α expression differed. The data are expressed as the mean ± standard deviation. Δ P

    Article Snippet: The membranes were subsequently treated with the appropriate antibodies against the following proteins: TGF-β1 (1/1000) (Cat# ab179695, Abcam, Shanghai, China), TGF-β2 (1/500) (Cat# 167655, Abcam, Shanghai, China), TNF-α (1/1000) (Cat# ab66579, Abcam, Shanghai, China), UCP-2 (1/500) (Cat# ab67241, Abcam, Shanghai, China), PPAR-α (1/1500) (Cat# GTX101098, GeneTex, Shanghai, China), PPAR-γ (1/2000) (Cat# ab191407, Abcam, Shanghai, China), LXR-α (1/1000) (Cat# ab41902, Abcam, Shanghai, China), ELOVL-2 (1/5000) (Cat# ab176327, Abcam, Shanghai, China) and β-actin (1/10000) (Cat# a5441, Sigma-Aldrich, Shanghai, China).

    Techniques: Expressing, Standard Deviation

    Hydrogen peroxide was critical for PLCγ-1 activation in UCP2 overexpressed cells Removal of hydrogen peroxide by catalase ( A ) suppressed lipid peroxidation ( B , N=4 per group), PLCγ-1 induction ( C , Fra-I is a subunit of the activator protein 1, which is activated during skin carcinogenesis) and the levels of its downstream targets: IP3 ( D , N=3 per group) and DAG ( E , N=3 per group), as well as 3D spheroid formation ( F , N=6 per group) of UCP2 overexpressed cells. *, p

    Journal: Molecular carcinogenesis

    Article Title: UCP2 Upregulation Promotes PLCγ-1 Signaling During Skin Cell Transformation

    doi: 10.1002/mc.22684

    Figure Lengend Snippet: Hydrogen peroxide was critical for PLCγ-1 activation in UCP2 overexpressed cells Removal of hydrogen peroxide by catalase ( A ) suppressed lipid peroxidation ( B , N=4 per group), PLCγ-1 induction ( C , Fra-I is a subunit of the activator protein 1, which is activated during skin carcinogenesis) and the levels of its downstream targets: IP3 ( D , N=3 per group) and DAG ( E , N=3 per group), as well as 3D spheroid formation ( F , N=6 per group) of UCP2 overexpressed cells. *, p

    Article Snippet: Superoxide is shown to activate UCP2, and in turn, elevated UCP2 decreases superoxide via a negative feedback loop [ – ].

    Techniques: Activation Assay

    Knockdown of PLCγ-1 inhibited fatty acid oxidation in UCP2 overexpressed cells (A) FAO was significantly higher in UCP2 overexpressed cells with palmitate compared to control pCMV cells. (B) siRNA knockdown of PLCγ-1 inhibited fatty acid oxidation in UCP2 overexpressed cells. *, p

    Journal: Molecular carcinogenesis

    Article Title: UCP2 Upregulation Promotes PLCγ-1 Signaling During Skin Cell Transformation

    doi: 10.1002/mc.22684

    Figure Lengend Snippet: Knockdown of PLCγ-1 inhibited fatty acid oxidation in UCP2 overexpressed cells (A) FAO was significantly higher in UCP2 overexpressed cells with palmitate compared to control pCMV cells. (B) siRNA knockdown of PLCγ-1 inhibited fatty acid oxidation in UCP2 overexpressed cells. *, p

    Article Snippet: Superoxide is shown to activate UCP2, and in turn, elevated UCP2 decreases superoxide via a negative feedback loop [ – ].

    Techniques:

    UCP2 enhanced lipid and protein oxidation Detection of lipid peroxidation by the MDA assay ( A, N=4 per group) and protein oxidation by Oxiblot ( B ) in UCP2 overexpressed and control JB6 cells. These cells were treated with TPA (5 nM) or vehicle control (DMSO) for 24 h. For Oxiblot, the bands were detected on the same gel but the lanes were not adjacent. *, p

    Journal: Molecular carcinogenesis

    Article Title: UCP2 Upregulation Promotes PLCγ-1 Signaling During Skin Cell Transformation

    doi: 10.1002/mc.22684

    Figure Lengend Snippet: UCP2 enhanced lipid and protein oxidation Detection of lipid peroxidation by the MDA assay ( A, N=4 per group) and protein oxidation by Oxiblot ( B ) in UCP2 overexpressed and control JB6 cells. These cells were treated with TPA (5 nM) or vehicle control (DMSO) for 24 h. For Oxiblot, the bands were detected on the same gel but the lanes were not adjacent. *, p

    Article Snippet: Superoxide is shown to activate UCP2, and in turn, elevated UCP2 decreases superoxide via a negative feedback loop [ – ].

    Techniques: Multiple Displacement Amplification

    UCP2 upregulation enhanced PLCγ-1 activation UCP2 knockout mice and wild-type (WT) mice were subjected to DMBA/TPA-induced skin carcinogenesis, and skin epidermal tissues were collected for this protein array analysis (21). Detection of p-PLCγ-1 ( A ) and Calmodulin ( B ) levels in skin tissue lysates. *, p

    Journal: Molecular carcinogenesis

    Article Title: UCP2 Upregulation Promotes PLCγ-1 Signaling During Skin Cell Transformation

    doi: 10.1002/mc.22684

    Figure Lengend Snippet: UCP2 upregulation enhanced PLCγ-1 activation UCP2 knockout mice and wild-type (WT) mice were subjected to DMBA/TPA-induced skin carcinogenesis, and skin epidermal tissues were collected for this protein array analysis (21). Detection of p-PLCγ-1 ( A ) and Calmodulin ( B ) levels in skin tissue lysates. *, p

    Article Snippet: Superoxide is shown to activate UCP2, and in turn, elevated UCP2 decreases superoxide via a negative feedback loop [ – ].

    Techniques: Activation Assay, Knock-Out, Mouse Assay, Protein Array

    UCP2 enhanced PLCγ-1 signaling The levels of IP3 ( A ), DAG ( B ), and intracellular calcium either by spectrophotometer ( C ) or fluorescent imaging ( D ) (Fluorescent imaging quantification results shown in E ) levels in UCP2 overexpressed cells and control JB6 cells. These cells were treated with TPA (5 nM) or vehicle control (DMSO) for 24 h. N=3 per group, data were presented as the mean ± SD.*, p

    Journal: Molecular carcinogenesis

    Article Title: UCP2 Upregulation Promotes PLCγ-1 Signaling During Skin Cell Transformation

    doi: 10.1002/mc.22684

    Figure Lengend Snippet: UCP2 enhanced PLCγ-1 signaling The levels of IP3 ( A ), DAG ( B ), and intracellular calcium either by spectrophotometer ( C ) or fluorescent imaging ( D ) (Fluorescent imaging quantification results shown in E ) levels in UCP2 overexpressed cells and control JB6 cells. These cells were treated with TPA (5 nM) or vehicle control (DMSO) for 24 h. N=3 per group, data were presented as the mean ± SD.*, p

    Article Snippet: Superoxide is shown to activate UCP2, and in turn, elevated UCP2 decreases superoxide via a negative feedback loop [ – ].

    Techniques: Spectrophotometry, Imaging

    UCP2 differentially regulates ROS production Control pCMV and UCP2 overexpressed JB6 P+ cells were treated with TPA (5 nM) or vehicle control (DMSO) for 24 h. Superoxide levels ( A ) were measured by quantifying the fluorescence of the dye MitoSox and hydrogen peroxide levels ( B ) were measured with the Amplex Red Hydrogen Peroxide Kit. ( C ) Measurement of manganese superoxide dismutase expression levels. The MnSOD/GAPDH bands were detected on the same gel but the lanes were not adjacent. The ratios of MnSOD/GAPDH were presented. MnSOD ( D ), GPx ( E ) and Catalase (F) activities were measured in pCMV and UCP2 cells. N=4 per group, data were presented as the mean ± SD. *, p

    Journal: Molecular carcinogenesis

    Article Title: UCP2 Upregulation Promotes PLCγ-1 Signaling During Skin Cell Transformation

    doi: 10.1002/mc.22684

    Figure Lengend Snippet: UCP2 differentially regulates ROS production Control pCMV and UCP2 overexpressed JB6 P+ cells were treated with TPA (5 nM) or vehicle control (DMSO) for 24 h. Superoxide levels ( A ) were measured by quantifying the fluorescence of the dye MitoSox and hydrogen peroxide levels ( B ) were measured with the Amplex Red Hydrogen Peroxide Kit. ( C ) Measurement of manganese superoxide dismutase expression levels. The MnSOD/GAPDH bands were detected on the same gel but the lanes were not adjacent. The ratios of MnSOD/GAPDH were presented. MnSOD ( D ), GPx ( E ) and Catalase (F) activities were measured in pCMV and UCP2 cells. N=4 per group, data were presented as the mean ± SD. *, p

    Article Snippet: Superoxide is shown to activate UCP2, and in turn, elevated UCP2 decreases superoxide via a negative feedback loop [ – ].

    Techniques: Fluorescence, Expressing

    The transfection and knockdown efficiency of siRNA against UCP2 in H9C2 cells. (A and B) H9C2 cells transfected with control siRNA (Cy3) emitted red fluorescence. The transfection efficiency is expressed as the ratio of the number of red fluorescence cells over all cells by fluorescence microscopy (magnification, x20). (C) The knockdown efficiency of siRNA against UCP2 in H9C2 cells. H9C2 cells were left untransfected (control), transfected with Lipofectamine 2000 (no siRNA), transfected with negative control siRNA (ncRNA), or transfected with siRNA1 or 2. After 24 h, the mRNA levels of uncoupling protein 2 (UCP2) were determined by RT-qPCR with normalization to 18s RNA. * P

    Journal: International Journal of Molecular Medicine

    Article Title: Silencing of uncoupling protein 2 by small interfering RNA aggravates mitochondrial dysfunction in cardiomyocytes under septic conditions

    doi: 10.3892/ijmm.2015.2177

    Figure Lengend Snippet: The transfection and knockdown efficiency of siRNA against UCP2 in H9C2 cells. (A and B) H9C2 cells transfected with control siRNA (Cy3) emitted red fluorescence. The transfection efficiency is expressed as the ratio of the number of red fluorescence cells over all cells by fluorescence microscopy (magnification, x20). (C) The knockdown efficiency of siRNA against UCP2 in H9C2 cells. H9C2 cells were left untransfected (control), transfected with Lipofectamine 2000 (no siRNA), transfected with negative control siRNA (ncRNA), or transfected with siRNA1 or 2. After 24 h, the mRNA levels of uncoupling protein 2 (UCP2) were determined by RT-qPCR with normalization to 18s RNA. * P

    Article Snippet: Research on the association between UCP2 and mtDNA in sepsis is limited, and the possible explanation of our finding is that the silencing of UCP2 through the alteration in ROS production, uncoupling activity and MMP, eventually leads to the deletion of mtDNA under septic conditions.

    Techniques: Transfection, Fluorescence, Microscopy, Negative Control, Quantitative RT-PCR

    Uncoupling protein 2 (UCP2) mRNA and protein levels in H9C2 cells. Total RNA was extracted and the relative (A and B) protein and (C) mRNA levels of UCP2 were determined by western blot analysis (β-actin was used as a loading control) and RT-qPCR (with normalization to 18s RNA), respectively. Values are the means ± SD; n=3 for each group. * P

    Journal: International Journal of Molecular Medicine

    Article Title: Silencing of uncoupling protein 2 by small interfering RNA aggravates mitochondrial dysfunction in cardiomyocytes under septic conditions

    doi: 10.3892/ijmm.2015.2177

    Figure Lengend Snippet: Uncoupling protein 2 (UCP2) mRNA and protein levels in H9C2 cells. Total RNA was extracted and the relative (A and B) protein and (C) mRNA levels of UCP2 were determined by western blot analysis (β-actin was used as a loading control) and RT-qPCR (with normalization to 18s RNA), respectively. Values are the means ± SD; n=3 for each group. * P

    Article Snippet: Research on the association between UCP2 and mtDNA in sepsis is limited, and the possible explanation of our finding is that the silencing of UCP2 through the alteration in ROS production, uncoupling activity and MMP, eventually leads to the deletion of mtDNA under septic conditions.

    Techniques: Western Blot, Quantitative RT-PCR

    Effect of UCP-2 knockdown on Bcl-2 expression and cyanide toxicity. Cells were transfected with UCP-2 RNAi and 24 h later treated with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 12 h. (A) Bcl-2 levels as detected by Western

    Journal: Toxicology and applied pharmacology

    Article Title: Cyanide-induced Death of Dopaminergic Cells is Mediated by Uncoupling Protein-2 Up-regulation and Reduced Bcl-2 Expression

    doi: 10.1016/j.taap.2009.03.020

    Figure Lengend Snippet: Effect of UCP-2 knockdown on Bcl-2 expression and cyanide toxicity. Cells were transfected with UCP-2 RNAi and 24 h later treated with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 12 h. (A) Bcl-2 levels as detected by Western

    Article Snippet: To determine whether the level of UCP-2 is linked with changes of Bcl-2 expression, UCP-2 was up-regulated by treatment with Wy14,643 and the subsequent expression level of Bcl-2 examined.

    Techniques: Expressing, Transfection, Western Blot

    Effect of Bcl-2 over-expression on cyanide toxicity following UCP-2 up-regulation. 24 h after transfection with a Bcl-2 + expression plasmid, cells were treated with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 24 h. (A) Cells

    Journal: Toxicology and applied pharmacology

    Article Title: Cyanide-induced Death of Dopaminergic Cells is Mediated by Uncoupling Protein-2 Up-regulation and Reduced Bcl-2 Expression

    doi: 10.1016/j.taap.2009.03.020

    Figure Lengend Snippet: Effect of Bcl-2 over-expression on cyanide toxicity following UCP-2 up-regulation. 24 h after transfection with a Bcl-2 + expression plasmid, cells were treated with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 24 h. (A) Cells

    Article Snippet: To determine whether the level of UCP-2 is linked with changes of Bcl-2 expression, UCP-2 was up-regulated by treatment with Wy14,643 and the subsequent expression level of Bcl-2 examined.

    Techniques: Over Expression, Transfection, Expressing, Plasmid Preparation

    Effect of UCP-2 up-regulation on cyanide-induced cell death. Cells were treated with Wy14,643 (100 μM) for 5 h to up-regulate UCP-2, followed by incubation with KCN (400 μM) for 24 h. Cell death was determined with Sytox green. (A) Representative

    Journal: Toxicology and applied pharmacology

    Article Title: Cyanide-induced Death of Dopaminergic Cells is Mediated by Uncoupling Protein-2 Up-regulation and Reduced Bcl-2 Expression

    doi: 10.1016/j.taap.2009.03.020

    Figure Lengend Snippet: Effect of UCP-2 up-regulation on cyanide-induced cell death. Cells were treated with Wy14,643 (100 μM) for 5 h to up-regulate UCP-2, followed by incubation with KCN (400 μM) for 24 h. Cell death was determined with Sytox green. (A) Representative

    Article Snippet: To determine whether the level of UCP-2 is linked with changes of Bcl-2 expression, UCP-2 was up-regulated by treatment with Wy14,643 and the subsequent expression level of Bcl-2 examined.

    Techniques: Incubation

    Effect of UCP-2 regulation on Bcl-2 expression. (A) Cells were treated with Wy14,643 (25–200 μM) for 12 h, and then UCP-2 and Bcl-2 expression determined by Western blot analysis. (B) Time course of UCP-2 and Bcl-2 expression after treatment

    Journal: Toxicology and applied pharmacology

    Article Title: Cyanide-induced Death of Dopaminergic Cells is Mediated by Uncoupling Protein-2 Up-regulation and Reduced Bcl-2 Expression

    doi: 10.1016/j.taap.2009.03.020

    Figure Lengend Snippet: Effect of UCP-2 regulation on Bcl-2 expression. (A) Cells were treated with Wy14,643 (25–200 μM) for 12 h, and then UCP-2 and Bcl-2 expression determined by Western blot analysis. (B) Time course of UCP-2 and Bcl-2 expression after treatment

    Article Snippet: To determine whether the level of UCP-2 is linked with changes of Bcl-2 expression, UCP-2 was up-regulated by treatment with Wy14,643 and the subsequent expression level of Bcl-2 examined.

    Techniques: Expressing, Western Blot

    Effect of cyanide on Bcl-2 expression after UCP-2 up-regulation or over-expression. (A) UCP-2 was up-regulated by Wy14,643 (100 μM) treatment for 5 h, followed by KCN (400 μM) for 12 h. Cellular Bcl-2 expression was determined by Western

    Journal: Toxicology and applied pharmacology

    Article Title: Cyanide-induced Death of Dopaminergic Cells is Mediated by Uncoupling Protein-2 Up-regulation and Reduced Bcl-2 Expression

    doi: 10.1016/j.taap.2009.03.020

    Figure Lengend Snippet: Effect of cyanide on Bcl-2 expression after UCP-2 up-regulation or over-expression. (A) UCP-2 was up-regulated by Wy14,643 (100 μM) treatment for 5 h, followed by KCN (400 μM) for 12 h. Cellular Bcl-2 expression was determined by Western

    Article Snippet: To determine whether the level of UCP-2 is linked with changes of Bcl-2 expression, UCP-2 was up-regulated by treatment with Wy14,643 and the subsequent expression level of Bcl-2 examined.

    Techniques: Expressing, Over Expression, Western Blot

    Effect of cyanide on Bcl-2 mRNA levels and proteasomal metabolism following UCP-2 up-regulation. (A) Bcl-2 mRNA expression was determined by real-time PCR analysis. (B) Western analysis of whole cell ubiquinated proteins was determined by blotting with

    Journal: Toxicology and applied pharmacology

    Article Title: Cyanide-induced Death of Dopaminergic Cells is Mediated by Uncoupling Protein-2 Up-regulation and Reduced Bcl-2 Expression

    doi: 10.1016/j.taap.2009.03.020

    Figure Lengend Snippet: Effect of cyanide on Bcl-2 mRNA levels and proteasomal metabolism following UCP-2 up-regulation. (A) Bcl-2 mRNA expression was determined by real-time PCR analysis. (B) Western analysis of whole cell ubiquinated proteins was determined by blotting with

    Article Snippet: To determine whether the level of UCP-2 is linked with changes of Bcl-2 expression, UCP-2 was up-regulated by treatment with Wy14,643 and the subsequent expression level of Bcl-2 examined.

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Western Blot

    Effect of UCP-2 knockdown on mtGSH levels and H 2 O 2 generation. Cells were transfected with UCP-2 RNAi and 24 h later treated with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 12 h. (A) Effect of UCP-2 RNAi on mtGSH levels. Control

    Journal: Toxicology and applied pharmacology

    Article Title: Cyanide-induced Death of Dopaminergic Cells is Mediated by Uncoupling Protein-2 Up-regulation and Reduced Bcl-2 Expression

    doi: 10.1016/j.taap.2009.03.020

    Figure Lengend Snippet: Effect of UCP-2 knockdown on mtGSH levels and H 2 O 2 generation. Cells were transfected with UCP-2 RNAi and 24 h later treated with Wy14,643 (100 μM) for 5 h, followed by KCN (400 μM) for 12 h. (A) Effect of UCP-2 RNAi on mtGSH levels. Control

    Article Snippet: To determine whether the level of UCP-2 is linked with changes of Bcl-2 expression, UCP-2 was up-regulated by treatment with Wy14,643 and the subsequent expression level of Bcl-2 examined.

    Techniques: Transfection

    Pretreatment with EPA or DHA prevents the doxorubicin-induced decrease in UCP2 protein expression. H9C2 cells were left untreated or were treated with 50 μM DHA or 100 μM EPA for 24 h, then were left untreated or wre treated with 1 μM doxorubicin (DOX) in the continued presence of the fatty acid for 24 h. After treatment, the cells were harvested and proteins extracted for Western blotting using antibody against UCP2 with ß-actin as the internal control. The bars are the quantitative density analysis expressed as the relative density compared to that in the untreated control and are the mean ± S.D. for three separate experiments. **, ***: p

    Journal: Journal of Biomedical Science

    Article Title: N-3 polyunsaturated fatty acids decrease levels of doxorubicin-induced reactive oxygen species in cardiomyocytes -- involvement of uncoupling protein UCP2

    doi: 10.1186/s12929-014-0101-3

    Figure Lengend Snippet: Pretreatment with EPA or DHA prevents the doxorubicin-induced decrease in UCP2 protein expression. H9C2 cells were left untreated or were treated with 50 μM DHA or 100 μM EPA for 24 h, then were left untreated or wre treated with 1 μM doxorubicin (DOX) in the continued presence of the fatty acid for 24 h. After treatment, the cells were harvested and proteins extracted for Western blotting using antibody against UCP2 with ß-actin as the internal control. The bars are the quantitative density analysis expressed as the relative density compared to that in the untreated control and are the mean ± S.D. for three separate experiments. **, ***: p

    Article Snippet: After transfer of the proteins from the gel to a nitrocellulose membrane (Amersham Pharmacia Biotech, Freiburg, Germany), the membranes were blocked for 1 h at room temperature in phosphate-buffered saline (PBS) containing 0.05% Tween 20 (PBS-T) and 5% nonfat dry milk, then were incubated with anti-UCP2 (Santa Cruz Bio.

    Techniques: Expressing, Western Blot

    EPA or DHA increases UCP2 mRNA levels in H9C2 cells. H9C2 cells were left untreated or were treated with 100 μM EPA or 50 μM DHA for 24 h, then UCP2 mRNA expression was measured by reverse transcription and quantitative real-time PCR, with GAPDH (glyceraldehyde-3-phosphate dehydrogenase) as the internal control. The results are expressed relative to the untreated control value and are the mean ± S.D. for three independent experiments. *: p

    Journal: Journal of Biomedical Science

    Article Title: N-3 polyunsaturated fatty acids decrease levels of doxorubicin-induced reactive oxygen species in cardiomyocytes -- involvement of uncoupling protein UCP2

    doi: 10.1186/s12929-014-0101-3

    Figure Lengend Snippet: EPA or DHA increases UCP2 mRNA levels in H9C2 cells. H9C2 cells were left untreated or were treated with 100 μM EPA or 50 μM DHA for 24 h, then UCP2 mRNA expression was measured by reverse transcription and quantitative real-time PCR, with GAPDH (glyceraldehyde-3-phosphate dehydrogenase) as the internal control. The results are expressed relative to the untreated control value and are the mean ± S.D. for three independent experiments. *: p

    Article Snippet: After transfer of the proteins from the gel to a nitrocellulose membrane (Amersham Pharmacia Biotech, Freiburg, Germany), the membranes were blocked for 1 h at room temperature in phosphate-buffered saline (PBS) containing 0.05% Tween 20 (PBS-T) and 5% nonfat dry milk, then were incubated with anti-UCP2 (Santa Cruz Bio.

    Techniques: Expressing, Real-time Polymerase Chain Reaction

    Pretreatment with EPA or DHA prevents the doxorubicin-induced decrease in UCP2 mRNA levels. H9C2 cells were (i) left untreated or (ii) treated with 100 μM EPA or 50 μM DHA for 24 h, then treated with 1 μM doxorubicin for 24 h or (iii) treated with 1 μM doxorubicin (DOX) in the absence or presence of 100 μM EPA or 50 μM DHA for 24 h, then UCP2 mRNA levels were measured by reverse transcription and quantitative real-time PCR, with GAPDH (glyceraldehyde-3-phosphate dehydrogenase) as the internal control. The results are expressed relative to the untreated control value and are the mean ± S.D. for three independent experiments. ***: p

    Journal: Journal of Biomedical Science

    Article Title: N-3 polyunsaturated fatty acids decrease levels of doxorubicin-induced reactive oxygen species in cardiomyocytes -- involvement of uncoupling protein UCP2

    doi: 10.1186/s12929-014-0101-3

    Figure Lengend Snippet: Pretreatment with EPA or DHA prevents the doxorubicin-induced decrease in UCP2 mRNA levels. H9C2 cells were (i) left untreated or (ii) treated with 100 μM EPA or 50 μM DHA for 24 h, then treated with 1 μM doxorubicin for 24 h or (iii) treated with 1 μM doxorubicin (DOX) in the absence or presence of 100 μM EPA or 50 μM DHA for 24 h, then UCP2 mRNA levels were measured by reverse transcription and quantitative real-time PCR, with GAPDH (glyceraldehyde-3-phosphate dehydrogenase) as the internal control. The results are expressed relative to the untreated control value and are the mean ± S.D. for three independent experiments. ***: p

    Article Snippet: After transfer of the proteins from the gel to a nitrocellulose membrane (Amersham Pharmacia Biotech, Freiburg, Germany), the membranes were blocked for 1 h at room temperature in phosphate-buffered saline (PBS) containing 0.05% Tween 20 (PBS-T) and 5% nonfat dry milk, then were incubated with anti-UCP2 (Santa Cruz Bio.

    Techniques: Real-time Polymerase Chain Reaction

    Doxorubicin decreases cell viability and UCP2 mRNA levels in H9C2 cells. H9C2 cells were left untreated or were treated with 0.5 or 1 μM doxorubicin (DOX) for 24 h, then (A) cell viability was measured by the MTT method and (B) UCP2 expression was measured by reverse transcription and quantitative real-time PCR, with GAPDH (glyceraldehyde-3-phosphate dehydrogenase) as the internal control. The results are expressed relative to the control value and are the mean ± S.D. for three independent experiments. *: p

    Journal: Journal of Biomedical Science

    Article Title: N-3 polyunsaturated fatty acids decrease levels of doxorubicin-induced reactive oxygen species in cardiomyocytes -- involvement of uncoupling protein UCP2

    doi: 10.1186/s12929-014-0101-3

    Figure Lengend Snippet: Doxorubicin decreases cell viability and UCP2 mRNA levels in H9C2 cells. H9C2 cells were left untreated or were treated with 0.5 or 1 μM doxorubicin (DOX) for 24 h, then (A) cell viability was measured by the MTT method and (B) UCP2 expression was measured by reverse transcription and quantitative real-time PCR, with GAPDH (glyceraldehyde-3-phosphate dehydrogenase) as the internal control. The results are expressed relative to the control value and are the mean ± S.D. for three independent experiments. *: p

    Article Snippet: After transfer of the proteins from the gel to a nitrocellulose membrane (Amersham Pharmacia Biotech, Freiburg, Germany), the membranes were blocked for 1 h at room temperature in phosphate-buffered saline (PBS) containing 0.05% Tween 20 (PBS-T) and 5% nonfat dry milk, then were incubated with anti-UCP2 (Santa Cruz Bio.

    Techniques: MTT Assay, Expressing, Real-time Polymerase Chain Reaction

    UCP2 suppression induced ABCG2 expression via ROS/Nrf2 in hypoxia-triggered NSCLC chemoresistance A . Western blot analysis of cells infected with lentiviruses expressing control or UCP2-targeted shRNAs in normoxia. B . Measurement of ROS levels in cells exposed to normoxia or hypoxia and treated with cisplatin (CP, 30 μM) or docetaxel (DTC, 10 μM). *, #P

    Journal: Oncotarget

    Article Title: Uncoupling protein 2 downregulation by hypoxia through repression of peroxisome proliferator-activated receptor γ promotes chemoresistance of non-small cell lung cancer

    doi: 10.18632/oncotarget.14097

    Figure Lengend Snippet: UCP2 suppression induced ABCG2 expression via ROS/Nrf2 in hypoxia-triggered NSCLC chemoresistance A . Western blot analysis of cells infected with lentiviruses expressing control or UCP2-targeted shRNAs in normoxia. B . Measurement of ROS levels in cells exposed to normoxia or hypoxia and treated with cisplatin (CP, 30 μM) or docetaxel (DTC, 10 μM). *, #P

    Article Snippet: Blotting was performed with antibodies against UCP2 (Clone # sc-6526, Santa Cruz, Dallas, USA), PPARγ (Cat. # 2443, Cell Signaling Technology, Boston, USA), DEC1 (Santa Cruz), HIF1α (Cat. # 14179, Cell Signaling), HIF-1β (Cat. # 3414, Cell Signaling), Stat3 (Cat. # 9139, Cell Signaling), phospho-Stat3 (Tyr705, Cat. # 9145, Cell Signaling), and ABCG2 (Cat. # 4477, Cell Signaling).

    Techniques: Expressing, Western Blot, Infection

    UCP2 downregulation contributed to NSCLC cell chemoresistance in hypoxia A . Representative UCP2 immunostaining of tumors from paired patients with NSCLC alone and NSCLC combined with COPD. Magnification, 200×; Scale bars, 100 μm. B . Representative immunohistochemical staining for UCP2 using carcinoma tissues from paired chemotherapy-sensitive and -resistant patients. Scale bars, 200μm (100×), 100 μm (200×) and 50μm (400×). C . Patients were grouped according to the expression of UCP2 in the carcinomas, and subjected to follow-up investigations. The percent of surviving patients was plotted. D . qRT-PCR assays of UCP2 levels in NSCLC cells exposed to the indicated concentrations of oxygen. E . Western blot analysis of NSCLC cells exposed to normoxia or hypoxia. F . Western blot analysis of cells transfected with UCP2-targeted or scrambled (NC) siRNAs or cells stably transfected with a control or UCP2-overexpressing construct. G, H . CCK8 assays for NSCLC cells infected with lentiviruses expressing control or UCP2-targeted shRNAs (G) or cells stably transfected with a control or UCP2-overexpressing construct (H). I . Colony formation assays for cisplatin (2 μM) or docetaxel (20 nM) treated NSCLC cells, which were infected with lentiviruses expressing control or UCP2-targeted shRNAs. J . Cisplatin (30 μM) induced apoptosis were investigated in NSCLC cells infected with lentiviruses expressing control or UCP2-targeted shRNAs with Annexin V/PI staining kit by flow cytometry assays. K . Cell scratch assays for NSCLC cells infected with lentiviruses expressing control or UCP2-targeted shRNAs. Unless indicated, cells were incubated and subjected to drug treatment in normoxia. Scale bars, 100 μm. Data are represented as the mean ± SEM of n = 3 replicates or representative of 3 independent experiments (A-J). * P

    Journal: Oncotarget

    Article Title: Uncoupling protein 2 downregulation by hypoxia through repression of peroxisome proliferator-activated receptor γ promotes chemoresistance of non-small cell lung cancer

    doi: 10.18632/oncotarget.14097

    Figure Lengend Snippet: UCP2 downregulation contributed to NSCLC cell chemoresistance in hypoxia A . Representative UCP2 immunostaining of tumors from paired patients with NSCLC alone and NSCLC combined with COPD. Magnification, 200×; Scale bars, 100 μm. B . Representative immunohistochemical staining for UCP2 using carcinoma tissues from paired chemotherapy-sensitive and -resistant patients. Scale bars, 200μm (100×), 100 μm (200×) and 50μm (400×). C . Patients were grouped according to the expression of UCP2 in the carcinomas, and subjected to follow-up investigations. The percent of surviving patients was plotted. D . qRT-PCR assays of UCP2 levels in NSCLC cells exposed to the indicated concentrations of oxygen. E . Western blot analysis of NSCLC cells exposed to normoxia or hypoxia. F . Western blot analysis of cells transfected with UCP2-targeted or scrambled (NC) siRNAs or cells stably transfected with a control or UCP2-overexpressing construct. G, H . CCK8 assays for NSCLC cells infected with lentiviruses expressing control or UCP2-targeted shRNAs (G) or cells stably transfected with a control or UCP2-overexpressing construct (H). I . Colony formation assays for cisplatin (2 μM) or docetaxel (20 nM) treated NSCLC cells, which were infected with lentiviruses expressing control or UCP2-targeted shRNAs. J . Cisplatin (30 μM) induced apoptosis were investigated in NSCLC cells infected with lentiviruses expressing control or UCP2-targeted shRNAs with Annexin V/PI staining kit by flow cytometry assays. K . Cell scratch assays for NSCLC cells infected with lentiviruses expressing control or UCP2-targeted shRNAs. Unless indicated, cells were incubated and subjected to drug treatment in normoxia. Scale bars, 100 μm. Data are represented as the mean ± SEM of n = 3 replicates or representative of 3 independent experiments (A-J). * P

    Article Snippet: Blotting was performed with antibodies against UCP2 (Clone # sc-6526, Santa Cruz, Dallas, USA), PPARγ (Cat. # 2443, Cell Signaling Technology, Boston, USA), DEC1 (Santa Cruz), HIF1α (Cat. # 14179, Cell Signaling), HIF-1β (Cat. # 3414, Cell Signaling), Stat3 (Cat. # 9139, Cell Signaling), phospho-Stat3 (Tyr705, Cat. # 9145, Cell Signaling), and ABCG2 (Cat. # 4477, Cell Signaling).

    Techniques: Immunostaining, Immunohistochemistry, Staining, Expressing, Quantitative RT-PCR, Western Blot, Transfection, Stable Transfection, Construct, Infection, Flow Cytometry, Cytometry, Incubation

    Hypoxia suppressed UCP2 via downregulation of PPAR-γ in NSCLCs A . Western blot analysis of cells pre-exposed to normoxia or hypoxia. B . Western blot analysis of cells transfected with siRNAs targeting different sites of the indicated mRNAs. The siRNAs with the highest silencing efficacy (#1 for PPAR-γ and #2 for STAT3) were used thereafter. C . Western blot analysis of cells transfected with scrambled siRNA or siRNA targeted to the indicated mRNAs. D . Western blot analysis of cells treated with vehicle or 4 μM rosiglitazone. E . CCK8 assays of cells transfected with scrambled or PPAR-γ-targeted siRNA. Data are represented as the mean ± SEM of n = 3 replicates or representative of 3 independent experiments. * P

    Journal: Oncotarget

    Article Title: Uncoupling protein 2 downregulation by hypoxia through repression of peroxisome proliferator-activated receptor γ promotes chemoresistance of non-small cell lung cancer

    doi: 10.18632/oncotarget.14097

    Figure Lengend Snippet: Hypoxia suppressed UCP2 via downregulation of PPAR-γ in NSCLCs A . Western blot analysis of cells pre-exposed to normoxia or hypoxia. B . Western blot analysis of cells transfected with siRNAs targeting different sites of the indicated mRNAs. The siRNAs with the highest silencing efficacy (#1 for PPAR-γ and #2 for STAT3) were used thereafter. C . Western blot analysis of cells transfected with scrambled siRNA or siRNA targeted to the indicated mRNAs. D . Western blot analysis of cells treated with vehicle or 4 μM rosiglitazone. E . CCK8 assays of cells transfected with scrambled or PPAR-γ-targeted siRNA. Data are represented as the mean ± SEM of n = 3 replicates or representative of 3 independent experiments. * P

    Article Snippet: Blotting was performed with antibodies against UCP2 (Clone # sc-6526, Santa Cruz, Dallas, USA), PPARγ (Cat. # 2443, Cell Signaling Technology, Boston, USA), DEC1 (Santa Cruz), HIF1α (Cat. # 14179, Cell Signaling), HIF-1β (Cat. # 3414, Cell Signaling), Stat3 (Cat. # 9139, Cell Signaling), phospho-Stat3 (Tyr705, Cat. # 9145, Cell Signaling), and ABCG2 (Cat. # 4477, Cell Signaling).

    Techniques: Western Blot, Transfection

    Hypoxia suppression of PPAR-γ and UCP2 was mediated by HIF-1α in NSCLC cells A . Western blot analysis of cells pre-exposed to normoxia or hypoxia. B . qRT-PCR assays for the expression of HIF-1 target genes. C, D . Cells were transfected with siRNAs against the indicated genes, exposed to hypoxia, and subjected to Western blot analysis. Data are represented as the mean ± SEM of n = 3 replicates or representative of 3 independent experiments. * P

    Journal: Oncotarget

    Article Title: Uncoupling protein 2 downregulation by hypoxia through repression of peroxisome proliferator-activated receptor γ promotes chemoresistance of non-small cell lung cancer

    doi: 10.18632/oncotarget.14097

    Figure Lengend Snippet: Hypoxia suppression of PPAR-γ and UCP2 was mediated by HIF-1α in NSCLC cells A . Western blot analysis of cells pre-exposed to normoxia or hypoxia. B . qRT-PCR assays for the expression of HIF-1 target genes. C, D . Cells were transfected with siRNAs against the indicated genes, exposed to hypoxia, and subjected to Western blot analysis. Data are represented as the mean ± SEM of n = 3 replicates or representative of 3 independent experiments. * P

    Article Snippet: Blotting was performed with antibodies against UCP2 (Clone # sc-6526, Santa Cruz, Dallas, USA), PPARγ (Cat. # 2443, Cell Signaling Technology, Boston, USA), DEC1 (Santa Cruz), HIF1α (Cat. # 14179, Cell Signaling), HIF-1β (Cat. # 3414, Cell Signaling), Stat3 (Cat. # 9139, Cell Signaling), phospho-Stat3 (Tyr705, Cat. # 9145, Cell Signaling), and ABCG2 (Cat. # 4477, Cell Signaling).

    Techniques: Western Blot, Quantitative RT-PCR, Expressing, Transfection

    UCP2 downregulation in hypoxia underlies metabolic reprogramming and apoptosis resistance of NSCLC cells A, B . Glucose consumption and lactate production assays of cells infected with lentiviruses expressing control or UCP2-targeted shRNAs in normoxia (A) or cells stably transfected with a control or UCP2-overexpressing construct (B). C . Western blot analysis of cells infected with lentiviruses expressing control or UCP2-targeted shRNAs prior to exposure to normoxia or hypoxia. D . A working model that summarizes the overall findings of this study. Hypoxia downregulates UCP2 by transcriptionally repressing PPAR-γ, which contributes to chemoresistance of NSCLC cells via ROS/Nrf2-mediated upregulation of ABCG2. Data are represented as the mean ± SEM of n = 3 replicates or representative of 3 independent experiments. * P

    Journal: Oncotarget

    Article Title: Uncoupling protein 2 downregulation by hypoxia through repression of peroxisome proliferator-activated receptor γ promotes chemoresistance of non-small cell lung cancer

    doi: 10.18632/oncotarget.14097

    Figure Lengend Snippet: UCP2 downregulation in hypoxia underlies metabolic reprogramming and apoptosis resistance of NSCLC cells A, B . Glucose consumption and lactate production assays of cells infected with lentiviruses expressing control or UCP2-targeted shRNAs in normoxia (A) or cells stably transfected with a control or UCP2-overexpressing construct (B). C . Western blot analysis of cells infected with lentiviruses expressing control or UCP2-targeted shRNAs prior to exposure to normoxia or hypoxia. D . A working model that summarizes the overall findings of this study. Hypoxia downregulates UCP2 by transcriptionally repressing PPAR-γ, which contributes to chemoresistance of NSCLC cells via ROS/Nrf2-mediated upregulation of ABCG2. Data are represented as the mean ± SEM of n = 3 replicates or representative of 3 independent experiments. * P

    Article Snippet: Blotting was performed with antibodies against UCP2 (Clone # sc-6526, Santa Cruz, Dallas, USA), PPARγ (Cat. # 2443, Cell Signaling Technology, Boston, USA), DEC1 (Santa Cruz), HIF1α (Cat. # 14179, Cell Signaling), HIF-1β (Cat. # 3414, Cell Signaling), Stat3 (Cat. # 9139, Cell Signaling), phospho-Stat3 (Tyr705, Cat. # 9145, Cell Signaling), and ABCG2 (Cat. # 4477, Cell Signaling).

    Techniques: Infection, Expressing, Stable Transfection, Transfection, Construct, Western Blot

    UCP2 promotes the stabilization of HIF-1α through regulation of mitochondrial respiration and oxygen content in tubular cells. a Representative images of mice kidney sections from UCP2 WT or KO mice 6 weeks after I/R with immunostaining for pimonidazole. Scale bars, 100 μm. b Immunoblot analysis for PHD2 in kidney tissue from UCP2 WT or KO mice 6 weeks after I/R or sham laparotomy. Tubulin served as the standard. * p

    Journal: Cell Death & Disease

    Article Title: UCP2-induced hypoxia promotes lipid accumulation and tubulointerstitial fibrosis during ischemic kidney injury

    doi: 10.1038/s41419-019-2219-4

    Figure Lengend Snippet: UCP2 promotes the stabilization of HIF-1α through regulation of mitochondrial respiration and oxygen content in tubular cells. a Representative images of mice kidney sections from UCP2 WT or KO mice 6 weeks after I/R with immunostaining for pimonidazole. Scale bars, 100 μm. b Immunoblot analysis for PHD2 in kidney tissue from UCP2 WT or KO mice 6 weeks after I/R or sham laparotomy. Tubulin served as the standard. * p

    Article Snippet: In brief, they were stained with UCP2 antibody (sc-6527; Santa Cruz Biotechnology), PPARα antibody (ab24509, Abcam, Cambridge, MA, US), CPT1α antibody (ab128568, Abcam), fibronectin antibody (F3648, Sigma Aldrich), or collagen I antibody (1310–01, Southern Biotech) using the Vector Mouse on Mouse (M.O.M.) immunodetection Kit, according to the manufacturer’s protocol (Vector Laboratories, Burlingame, CA).

    Techniques: Mouse Assay, Immunostaining

    Deficiency of UCP2 protects against I/R-induced TIF. a Representative images of human kidney sections with or without tubulointerstitial fibrosis with immunostaining for UCP2. Scale bars, 100 μm. b Representative images of mice kidney sections from sham, I/R, FAN, and AAN mice with immunostaining for UCP2. Scale bars, 50 μm. c Immunoblot analysis of UCP2 in kidney tissue from mice 6 weeks after I/R or sham laparotomy. Voltage-dependent anion channel (VDAC) served as the standard. * p

    Journal: Cell Death & Disease

    Article Title: UCP2-induced hypoxia promotes lipid accumulation and tubulointerstitial fibrosis during ischemic kidney injury

    doi: 10.1038/s41419-019-2219-4

    Figure Lengend Snippet: Deficiency of UCP2 protects against I/R-induced TIF. a Representative images of human kidney sections with or without tubulointerstitial fibrosis with immunostaining for UCP2. Scale bars, 100 μm. b Representative images of mice kidney sections from sham, I/R, FAN, and AAN mice with immunostaining for UCP2. Scale bars, 50 μm. c Immunoblot analysis of UCP2 in kidney tissue from mice 6 weeks after I/R or sham laparotomy. Voltage-dependent anion channel (VDAC) served as the standard. * p

    Article Snippet: In brief, they were stained with UCP2 antibody (sc-6527; Santa Cruz Biotechnology), PPARα antibody (ab24509, Abcam, Cambridge, MA, US), CPT1α antibody (ab128568, Abcam), fibronectin antibody (F3648, Sigma Aldrich), or collagen I antibody (1310–01, Southern Biotech) using the Vector Mouse on Mouse (M.O.M.) immunodetection Kit, according to the manufacturer’s protocol (Vector Laboratories, Burlingame, CA).

    Techniques: Immunostaining, Mouse Assay

    Deficiency of UCP2 inhibits lipid accumulation. a – d Lipid in kidney tissue was determined in UCP2 WT or KO mice 6 weeks after I/R or sham laparotomy. Representative images of mice kidney sections with bodipy and Oil red O staining a , score of bodipy positive area b , quantification of Oil red O positive area c , and triglycerides contents kidney tissue d ; n = 7 per group. * p

    Journal: Cell Death & Disease

    Article Title: UCP2-induced hypoxia promotes lipid accumulation and tubulointerstitial fibrosis during ischemic kidney injury

    doi: 10.1038/s41419-019-2219-4

    Figure Lengend Snippet: Deficiency of UCP2 inhibits lipid accumulation. a – d Lipid in kidney tissue was determined in UCP2 WT or KO mice 6 weeks after I/R or sham laparotomy. Representative images of mice kidney sections with bodipy and Oil red O staining a , score of bodipy positive area b , quantification of Oil red O positive area c , and triglycerides contents kidney tissue d ; n = 7 per group. * p

    Article Snippet: In brief, they were stained with UCP2 antibody (sc-6527; Santa Cruz Biotechnology), PPARα antibody (ab24509, Abcam, Cambridge, MA, US), CPT1α antibody (ab128568, Abcam), fibronectin antibody (F3648, Sigma Aldrich), or collagen I antibody (1310–01, Southern Biotech) using the Vector Mouse on Mouse (M.O.M.) immunodetection Kit, according to the manufacturer’s protocol (Vector Laboratories, Burlingame, CA).

    Techniques: Mouse Assay, Staining

    UCP2 regulates HIF-1α expression. a Immunoblot analysis for HIF-1α in kidney tissue from UCP2 WT or KO mice 6 weeks after I/R or sham laparotomy. Tubulin served as the standard. * p

    Journal: Cell Death & Disease

    Article Title: UCP2-induced hypoxia promotes lipid accumulation and tubulointerstitial fibrosis during ischemic kidney injury

    doi: 10.1038/s41419-019-2219-4

    Figure Lengend Snippet: UCP2 regulates HIF-1α expression. a Immunoblot analysis for HIF-1α in kidney tissue from UCP2 WT or KO mice 6 weeks after I/R or sham laparotomy. Tubulin served as the standard. * p

    Article Snippet: In brief, they were stained with UCP2 antibody (sc-6527; Santa Cruz Biotechnology), PPARα antibody (ab24509, Abcam, Cambridge, MA, US), CPT1α antibody (ab128568, Abcam), fibronectin antibody (F3648, Sigma Aldrich), or collagen I antibody (1310–01, Southern Biotech) using the Vector Mouse on Mouse (M.O.M.) immunodetection Kit, according to the manufacturer’s protocol (Vector Laboratories, Burlingame, CA).

    Techniques: Expressing, Mouse Assay

    UCP2 regulates ECM production and lipid accumulation in primarily cultured PTCs. a Immunoblot analysis for fibronectin or collagen I of cell lysates from UCP2 WT or KO PTCs treated with hypoxia for 12 h, followed by reoxygenation for 12 h (H/R). Tubulin served as the standard. * p

    Journal: Cell Death & Disease

    Article Title: UCP2-induced hypoxia promotes lipid accumulation and tubulointerstitial fibrosis during ischemic kidney injury

    doi: 10.1038/s41419-019-2219-4

    Figure Lengend Snippet: UCP2 regulates ECM production and lipid accumulation in primarily cultured PTCs. a Immunoblot analysis for fibronectin or collagen I of cell lysates from UCP2 WT or KO PTCs treated with hypoxia for 12 h, followed by reoxygenation for 12 h (H/R). Tubulin served as the standard. * p

    Article Snippet: In brief, they were stained with UCP2 antibody (sc-6527; Santa Cruz Biotechnology), PPARα antibody (ab24509, Abcam, Cambridge, MA, US), CPT1α antibody (ab128568, Abcam), fibronectin antibody (F3648, Sigma Aldrich), or collagen I antibody (1310–01, Southern Biotech) using the Vector Mouse on Mouse (M.O.M.) immunodetection Kit, according to the manufacturer’s protocol (Vector Laboratories, Burlingame, CA).

    Techniques: Cell Culture

    Correlation between uncoupling protein 2 and uncoupling protein 2 mRNA expressions in human colon cancer. UCP2: Uncoupling protein 2; T: Tumour; P: Peritumoral.

    Journal: World Journal of Gastroenterology : WJG

    Article Title: Mitochondrial uncoupling protein 2 expression in colon cancer and its clinical significance

    doi: 10.3748/wjg.v16.i45.5773

    Figure Lengend Snippet: Correlation between uncoupling protein 2 and uncoupling protein 2 mRNA expressions in human colon cancer. UCP2: Uncoupling protein 2; T: Tumour; P: Peritumoral.

    Article Snippet: Immunoblots were developed using anti-UCP2 antibody (C-20; Santa Cruz Biotechnology, Inc, USA).

    Techniques:

    Mutant p53 inhibits UCP2 and PGC-1α through the inhibition of SESN1/AMPK signaling. a MDA-MB-231 cells were transduced with lentiviruses containing p53-SH1 or p53-SH2 vectors for mutant p53 silencing or their non-targeting negative control (NT). Left panel: western blotting was performed using 50 μg of whole-protein extracts and probed with the indicated antibodies. The p53 expression was shown as control of p53 knockdown efficacy and the GAPDH expression was used as control of equal proteins loading. Right panel: AMPK was immunoprecipitated from protein extracts using anti-rabbit AMPK antibody (IP: AMPK) and western blot analysis was performed using indicated antibodies. Protein extracts from cells silenced for p53 expression with p53-SH1 or p53-SH2 vectors were also immunoprecipitated with rabbit IgG as control. The blot exhibits equivalent AMPK levels in all samples. b H1299 p53-null cells stably expressing R273H mutant p53 (clone H1) and its respective mock control (clone C9) were used to confirm the regulation of SESN1:AMPK by mutant p53. Left panel: western blotting was performed using 50 μg of whole-protein extracts and probed with the indicated antibodies. Right panel: SESN1 was immunoprecipitated from protein extracts using anti-SESN1 antibody (IP: SESN1) and western blot analysis was performed using indicated antibodies. Protein extracts were also immunoprecipitated with IgG as con trol. c AsPC1-p53 null cells were transfected with the vectors for the ectopic expression of p53-R273H and its mock control and treated with 1 mM AICA-R for 48 h. Gene expression analysis of the UCP2 and PGC-1α was performed by RT-qPCR and normalized to GAPDH mRNA. # p

    Journal: British Journal of Cancer

    Article Title: Mutant p53 blocks SESN1/AMPK/PGC-1α/UCP2 axis increasing mitochondrial O2ˉ· production in cancer cells

    doi: 10.1038/s41416-018-0288-2

    Figure Lengend Snippet: Mutant p53 inhibits UCP2 and PGC-1α through the inhibition of SESN1/AMPK signaling. a MDA-MB-231 cells were transduced with lentiviruses containing p53-SH1 or p53-SH2 vectors for mutant p53 silencing or their non-targeting negative control (NT). Left panel: western blotting was performed using 50 μg of whole-protein extracts and probed with the indicated antibodies. The p53 expression was shown as control of p53 knockdown efficacy and the GAPDH expression was used as control of equal proteins loading. Right panel: AMPK was immunoprecipitated from protein extracts using anti-rabbit AMPK antibody (IP: AMPK) and western blot analysis was performed using indicated antibodies. Protein extracts from cells silenced for p53 expression with p53-SH1 or p53-SH2 vectors were also immunoprecipitated with rabbit IgG as control. The blot exhibits equivalent AMPK levels in all samples. b H1299 p53-null cells stably expressing R273H mutant p53 (clone H1) and its respective mock control (clone C9) were used to confirm the regulation of SESN1:AMPK by mutant p53. Left panel: western blotting was performed using 50 μg of whole-protein extracts and probed with the indicated antibodies. Right panel: SESN1 was immunoprecipitated from protein extracts using anti-SESN1 antibody (IP: SESN1) and western blot analysis was performed using indicated antibodies. Protein extracts were also immunoprecipitated with IgG as con trol. c AsPC1-p53 null cells were transfected with the vectors for the ectopic expression of p53-R273H and its mock control and treated with 1 mM AICA-R for 48 h. Gene expression analysis of the UCP2 and PGC-1α was performed by RT-qPCR and normalized to GAPDH mRNA. # p

    Article Snippet: UCP2 overexpression was performed using a pCMV expression vector containing the human complementary DNA of UCP2 (OriGene Technologies, Rockville, MD, USA).

    Techniques: Mutagenesis, Pyrolysis Gas Chromatography, Inhibition, Multiple Displacement Amplification, Transduction, Negative Control, Western Blot, Expressing, Immunoprecipitation, Stable Transfection, Transfection, Quantitative RT-PCR

    Mitochondrial superoxide production is due to mutp53-dependent UCP2 inhibition. a Panc1 mutR273H-p53 and AsPC1-p53 null cells were transfected with pRSuper-p53 and vector for mutant p53 ectopic expression, respectively, and their relative controls. In addition, Panc1 cells were co-transfected with siRNA-UCP2, or treated with 150 μM genipin for 24 h; while AsPC1 cells were co-transfected with the UCP2 vector. ROS production, corresponding to DCF fluorescence intensity, was analyzed by a multimode plate reader. * p

    Journal: British Journal of Cancer

    Article Title: Mutant p53 blocks SESN1/AMPK/PGC-1α/UCP2 axis increasing mitochondrial O2ˉ· production in cancer cells

    doi: 10.1038/s41416-018-0288-2

    Figure Lengend Snippet: Mitochondrial superoxide production is due to mutp53-dependent UCP2 inhibition. a Panc1 mutR273H-p53 and AsPC1-p53 null cells were transfected with pRSuper-p53 and vector for mutant p53 ectopic expression, respectively, and their relative controls. In addition, Panc1 cells were co-transfected with siRNA-UCP2, or treated with 150 μM genipin for 24 h; while AsPC1 cells were co-transfected with the UCP2 vector. ROS production, corresponding to DCF fluorescence intensity, was analyzed by a multimode plate reader. * p

    Article Snippet: UCP2 overexpression was performed using a pCMV expression vector containing the human complementary DNA of UCP2 (OriGene Technologies, Rockville, MD, USA).

    Techniques: Inhibition, Transfection, Plasmid Preparation, Mutagenesis, Expressing, Fluorescence

    Gemcitabine triggers WTp53 and UCP2 expression. a PaCa3 cells (WTp53) were transfected for 48 h with the pRSuper-p53 vector or its relative negative control (shCTRL). Gene expression analysis of p53, UCP2, and PGC-1α was performed by RT-qPCR and normalized to GAPDH mRNA. Protein expression analysis of p53, PGC-1α, UCP2, and GAPDH was performed by western blotting. * p

    Journal: British Journal of Cancer

    Article Title: Mutant p53 blocks SESN1/AMPK/PGC-1α/UCP2 axis increasing mitochondrial O2ˉ· production in cancer cells

    doi: 10.1038/s41416-018-0288-2

    Figure Lengend Snippet: Gemcitabine triggers WTp53 and UCP2 expression. a PaCa3 cells (WTp53) were transfected for 48 h with the pRSuper-p53 vector or its relative negative control (shCTRL). Gene expression analysis of p53, UCP2, and PGC-1α was performed by RT-qPCR and normalized to GAPDH mRNA. Protein expression analysis of p53, PGC-1α, UCP2, and GAPDH was performed by western blotting. * p

    Article Snippet: UCP2 overexpression was performed using a pCMV expression vector containing the human complementary DNA of UCP2 (OriGene Technologies, Rockville, MD, USA).

    Techniques: Expressing, Transfection, Plasmid Preparation, Negative Control, Pyrolysis Gas Chromatography, Quantitative RT-PCR, Western Blot

    Mutant p53 increases ΔΨm without damaging mtDNA. a Melanoma cell lines A375 (WTp53) and MeWo (mutant p53) were transfected with control or siRNA-p53. H 2 O 2 production was evaluated with the Amplex Red Kit, whereas UCP2 and p53 levels were determined by RT-qPCR. * p

    Journal: British Journal of Cancer

    Article Title: Mutant p53 blocks SESN1/AMPK/PGC-1α/UCP2 axis increasing mitochondrial O2ˉ· production in cancer cells

    doi: 10.1038/s41416-018-0288-2

    Figure Lengend Snippet: Mutant p53 increases ΔΨm without damaging mtDNA. a Melanoma cell lines A375 (WTp53) and MeWo (mutant p53) were transfected with control or siRNA-p53. H 2 O 2 production was evaluated with the Amplex Red Kit, whereas UCP2 and p53 levels were determined by RT-qPCR. * p

    Article Snippet: UCP2 overexpression was performed using a pCMV expression vector containing the human complementary DNA of UCP2 (OriGene Technologies, Rockville, MD, USA).

    Techniques: Mutagenesis, Transfection, Quantitative RT-PCR

    Mutant p53 downregulates UCP2 and PGC-1-α. a Panc1 mutR273H-p53 and AsPC1-p53 null cells were transfected with pRSuper-p53 vector and with plasmids for the ectopic expression of mutant p53-R273H or its relative negative control (CTRL). Gene expression analysis of the p53, UCP2, and PGC-1α was performed by RT-qPCR and was normalized to GAPDH mRNA. * p

    Journal: British Journal of Cancer

    Article Title: Mutant p53 blocks SESN1/AMPK/PGC-1α/UCP2 axis increasing mitochondrial O2ˉ· production in cancer cells

    doi: 10.1038/s41416-018-0288-2

    Figure Lengend Snippet: Mutant p53 downregulates UCP2 and PGC-1-α. a Panc1 mutR273H-p53 and AsPC1-p53 null cells were transfected with pRSuper-p53 vector and with plasmids for the ectopic expression of mutant p53-R273H or its relative negative control (CTRL). Gene expression analysis of the p53, UCP2, and PGC-1α was performed by RT-qPCR and was normalized to GAPDH mRNA. * p

    Article Snippet: UCP2 overexpression was performed using a pCMV expression vector containing the human complementary DNA of UCP2 (OriGene Technologies, Rockville, MD, USA).

    Techniques: Mutagenesis, Pyrolysis Gas Chromatography, Transfection, Plasmid Preparation, Expressing, Negative Control, Quantitative RT-PCR

    Wld S downregulates UCP2 expression and upregulates ATP levels through SIRT1. A : Wld S colocalized with SIRT1 in MIN6 cells. The stable cell lines expressing EGFP-Wld S were transiently transfected with pCMV-myc-SIRT1 and stained with anti-Myc antibody and DAPI. Scale bar, 5 μm. B : Wld S was coimmunoprecipitated with SIRT1 from the pancreatic lysates of Wld S mice. C : Wld S and its enzyme-dead mutant Wld S -H112A coimmunoprecipitated with SIRT1. The MIN6 cells stably expressing EGFP, EGFP-Wld S , or EGFP-Wld S -H112A were used for immunoprecipitation. UCP2 protein levels were also detected by Western blot. D and E : Liquid chromatography-tandem mass spectrometry analysis of NMN, NADP, NADPH, NAD, NADH, NA, and NAM extracted from pancreas of 9-week-old wild-type (WT) ( D ) or Wld S mice ( E ). *With significant difference. F : Quantification of the small molecules corresponding to D and E showed that NAD and NMN levels were upregulated in the pancreas of Wld S mice ( n = 4 for each genotype). G : Wld S repressed UCP2 promoter activity like SIRT1. UCP2 promoter activity was measured by luciferase assay in 293T cells transfected with pGL3-UCP2-Promoter and the indicated plasmids. H : Wld S downregulated UCP2 mRNA levels dependent on its enzyme activity. UCP2 mRNA level was measured by real-time PCR with MIN6 cell lines stably expressing EGFP, EGFP-Wld S , and EGFP-Wld S -H112A. I : Wld S downregulated UCP2 mRNA levels via SIRT1. UCP2 mRNA levels were determined by real-time PCR using islets isolated from mice with the indicated genotype ( n = 4 for each genotype). J : Wld S downregulated UCP2 protein levels via SIRT1. The protein levels in brown fat tissue with the indicated genotype were detected with SIRT1, Wld S , UCP2, and tubulin antibodies ( n = 3 for each genotype). K : Quantification of the UCP2 protein levels corresponding to J . L : Wld S increased ATP levels in primary cultured islets at the indicated glucose concentration ( n = 3). M : Wld S upregulated ATP level in islets via SIRT1. ATP levels were measured in islets with indicated genotypes at 2 mmol/L or 20 mmol/L glucose ( n = 3). * P

    Journal: Diabetes

    Article Title: WldS Enhances Insulin Transcription and Secretion via a SIRT1-Dependent Pathway and Improves Glucose Homeostasis

    doi: 10.2337/db11-0232

    Figure Lengend Snippet: Wld S downregulates UCP2 expression and upregulates ATP levels through SIRT1. A : Wld S colocalized with SIRT1 in MIN6 cells. The stable cell lines expressing EGFP-Wld S were transiently transfected with pCMV-myc-SIRT1 and stained with anti-Myc antibody and DAPI. Scale bar, 5 μm. B : Wld S was coimmunoprecipitated with SIRT1 from the pancreatic lysates of Wld S mice. C : Wld S and its enzyme-dead mutant Wld S -H112A coimmunoprecipitated with SIRT1. The MIN6 cells stably expressing EGFP, EGFP-Wld S , or EGFP-Wld S -H112A were used for immunoprecipitation. UCP2 protein levels were also detected by Western blot. D and E : Liquid chromatography-tandem mass spectrometry analysis of NMN, NADP, NADPH, NAD, NADH, NA, and NAM extracted from pancreas of 9-week-old wild-type (WT) ( D ) or Wld S mice ( E ). *With significant difference. F : Quantification of the small molecules corresponding to D and E showed that NAD and NMN levels were upregulated in the pancreas of Wld S mice ( n = 4 for each genotype). G : Wld S repressed UCP2 promoter activity like SIRT1. UCP2 promoter activity was measured by luciferase assay in 293T cells transfected with pGL3-UCP2-Promoter and the indicated plasmids. H : Wld S downregulated UCP2 mRNA levels dependent on its enzyme activity. UCP2 mRNA level was measured by real-time PCR with MIN6 cell lines stably expressing EGFP, EGFP-Wld S , and EGFP-Wld S -H112A. I : Wld S downregulated UCP2 mRNA levels via SIRT1. UCP2 mRNA levels were determined by real-time PCR using islets isolated from mice with the indicated genotype ( n = 4 for each genotype). J : Wld S downregulated UCP2 protein levels via SIRT1. The protein levels in brown fat tissue with the indicated genotype were detected with SIRT1, Wld S , UCP2, and tubulin antibodies ( n = 3 for each genotype). K : Quantification of the UCP2 protein levels corresponding to J . L : Wld S increased ATP levels in primary cultured islets at the indicated glucose concentration ( n = 3). M : Wld S upregulated ATP level in islets via SIRT1. ATP levels were measured in islets with indicated genotypes at 2 mmol/L or 20 mmol/L glucose ( n = 3). * P

    Article Snippet: In addition, WldS promoted insulin secretion and downregulated UCP2 via SIRT1 ( and ), which consisted with the studies that both β-cell–specific SIRT1-overexpressing mice and UCP2 knockout mice showed enhanced insulin secretion and resistance to HF diet–induced glucose intolerance ( , ).

    Techniques: Expressing, Stable Transfection, Transfection, Staining, Mouse Assay, Mutagenesis, Immunoprecipitation, Western Blot, Liquid Chromatography, Mass Spectrometry, Activity Assay, Luciferase, Real-time Polymerase Chain Reaction, Isolation, Cell Culture, Concentration Assay

    DCA increases mitochondrial OXPHOS and ROS production in A2780 cells compared with A2780/DDP cells. Notes: Mitochondrial citrate ( A ) and the OCR ( B ) were measured in the presence of DCA at the indicated doses for 24 hours. Mitochondrial ROS ( C ) and overall ROS ( E ) were detected in A2780 and A2780/DDP cells treated with DCA at the indicated doses for 24 hours by measuring fluorescence intensities using fluorescence microscopy (×200) or flow cytometry, respectively. ( D ) Expression levels of UCP2 protein in A2780 and A2780/DDP cells after DCA treatment. Data are presented as mean ± SE, n=3. * P

    Journal: OncoTargets and therapy

    Article Title: Dichloroacetic acid upregulates apoptosis of ovarian cancer cells by regulating mitochondrial function

    doi: 10.2147/OTT.S194329

    Figure Lengend Snippet: DCA increases mitochondrial OXPHOS and ROS production in A2780 cells compared with A2780/DDP cells. Notes: Mitochondrial citrate ( A ) and the OCR ( B ) were measured in the presence of DCA at the indicated doses for 24 hours. Mitochondrial ROS ( C ) and overall ROS ( E ) were detected in A2780 and A2780/DDP cells treated with DCA at the indicated doses for 24 hours by measuring fluorescence intensities using fluorescence microscopy (×200) or flow cytometry, respectively. ( D ) Expression levels of UCP2 protein in A2780 and A2780/DDP cells after DCA treatment. Data are presented as mean ± SE, n=3. * P

    Article Snippet: Anti-caspase-3 (1:1,000), anti-poly (ADP)-ribose polymerase (PARP) (1:2,000), anti-Bcl-2 (1:1,000), and anti-Bax (1:1,000) antibodies were from Santa Cruz Biotechnology (Santa Cruz, CA, USA); anti-PDK1, anti-PDH (1:1,000), anti-p-PDH (1:500), and anti-UCP2 (1:1,000) antibodies were from Abcam Biotechnology (Cambridge, MA, USA).

    Techniques: Fluorescence, Microscopy, Flow Cytometry, Cytometry, Expressing

    Cell viability and expression of UCP2 in A2780 and A2780/DDP cells after gene silencing of PDK1 combined with DCA. Notes: ( A ) shPDK1 combined with DCA further decreased the survival rate of A2780 cells, whereas there was no obvious effect in A2780/DDP cells. ( B ) The expression of UCP2 protein in shPDK1 A2780 cells and A2780/DDP cells. Data were expressed relative to the control group. * P

    Journal: OncoTargets and therapy

    Article Title: Dichloroacetic acid upregulates apoptosis of ovarian cancer cells by regulating mitochondrial function

    doi: 10.2147/OTT.S194329

    Figure Lengend Snippet: Cell viability and expression of UCP2 in A2780 and A2780/DDP cells after gene silencing of PDK1 combined with DCA. Notes: ( A ) shPDK1 combined with DCA further decreased the survival rate of A2780 cells, whereas there was no obvious effect in A2780/DDP cells. ( B ) The expression of UCP2 protein in shPDK1 A2780 cells and A2780/DDP cells. Data were expressed relative to the control group. * P

    Article Snippet: Anti-caspase-3 (1:1,000), anti-poly (ADP)-ribose polymerase (PARP) (1:2,000), anti-Bcl-2 (1:1,000), and anti-Bax (1:1,000) antibodies were from Santa Cruz Biotechnology (Santa Cruz, CA, USA); anti-PDK1, anti-PDH (1:1,000), anti-p-PDH (1:500), and anti-UCP2 (1:1,000) antibodies were from Abcam Biotechnology (Cambridge, MA, USA).

    Techniques: Expressing

    Identification of HOTTIP target genes regulated by canonical HOTTIP-HOXA13 axis. A , Expression levels of HOTTIP target genes in PDAC cells treated with siHOXA13 (n=3). B , Western blot analysis of HOTTIP targets in PANC-1 cells treated with siHOXA13. C , ChIP analysis of HOXA13 binding to the promoter of HOTTIP target genes (n=3). D-F , HOXA13 occupancy to the promoter of CHI3L1, CLIC5, CYP26B1 and UCP2 after knockdown of ( D ) HOTTIP and ( E ) HOXA13 in PDAC cells (n=3); and ( F ) after overexpression of HOTTIP in HPDE cells (n=3). *P

    Journal: bioRxiv

    Article Title: Ectopic HOTTIP Expression Induces Non-canonical Transactivation Pathways to Promote Growth and Invasiveness in Pancreatic Ductal Adenocarcinoma

    doi: 10.1101/812800

    Figure Lengend Snippet: Identification of HOTTIP target genes regulated by canonical HOTTIP-HOXA13 axis. A , Expression levels of HOTTIP target genes in PDAC cells treated with siHOXA13 (n=3). B , Western blot analysis of HOTTIP targets in PANC-1 cells treated with siHOXA13. C , ChIP analysis of HOXA13 binding to the promoter of HOTTIP target genes (n=3). D-F , HOXA13 occupancy to the promoter of CHI3L1, CLIC5, CYP26B1 and UCP2 after knockdown of ( D ) HOTTIP and ( E ) HOXA13 in PDAC cells (n=3); and ( F ) after overexpression of HOTTIP in HPDE cells (n=3). *P

    Article Snippet: Proteins were separated by SDS-PAGE, transferred to PVDF membrane and immunoblotted overnight at 4 °C with 1:1000 primary antibodies against HOXA13 (ab106503; abcam), MLL1 (#ABE240; Millipore), MLL2 (#ABE206, Millipore), MLL4 (NB600-254, Novus Biologicals), WDR5 (ab56919; abcam), CYB5R2 (H00051700-B02P; abnova), CYP26B1 (H00056603-M01; abnova), UCP2 (ab97931; abcam) and GAPDH (#5174; Cell signaling).

    Techniques: Expressing, Western Blot, Chromatin Immunoprecipitation, Binding Assay, Over Expression

    Schematic diagram describing the role of miR497-HOTTIP in the development and progression of PDAC. In PDAC, HOTTIP, which was inhibited by miR-497, was overexpressed. HOTTIP promoted PDAC development via canonical HOTTIP-HOXA13 axis and non-canonical trans -acting HOTTIP-WDR5-MLL1 complex. In HOTTIP-HOXA13 axis, HOTTIP activated the expression of HOXA13 which in turn activated CYP26B1, CLIC5, CHI3L1 and UCP2. In HOTTIP-WDR5-MLL1 pathway, HOTTIP-WDR5-MLL1 complex directly activated CYB5R2, SULT1A1, KIF26A, SLC1A4 and TSC22D1 in different chromosomes, without the involvement of HOXA13. These pathways resulted in enhanced cell growth and invasion in PDAC.

    Journal: bioRxiv

    Article Title: Ectopic HOTTIP Expression Induces Non-canonical Transactivation Pathways to Promote Growth and Invasiveness in Pancreatic Ductal Adenocarcinoma

    doi: 10.1101/812800

    Figure Lengend Snippet: Schematic diagram describing the role of miR497-HOTTIP in the development and progression of PDAC. In PDAC, HOTTIP, which was inhibited by miR-497, was overexpressed. HOTTIP promoted PDAC development via canonical HOTTIP-HOXA13 axis and non-canonical trans -acting HOTTIP-WDR5-MLL1 complex. In HOTTIP-HOXA13 axis, HOTTIP activated the expression of HOXA13 which in turn activated CYP26B1, CLIC5, CHI3L1 and UCP2. In HOTTIP-WDR5-MLL1 pathway, HOTTIP-WDR5-MLL1 complex directly activated CYB5R2, SULT1A1, KIF26A, SLC1A4 and TSC22D1 in different chromosomes, without the involvement of HOXA13. These pathways resulted in enhanced cell growth and invasion in PDAC.

    Article Snippet: Proteins were separated by SDS-PAGE, transferred to PVDF membrane and immunoblotted overnight at 4 °C with 1:1000 primary antibodies against HOXA13 (ab106503; abcam), MLL1 (#ABE240; Millipore), MLL2 (#ABE206, Millipore), MLL4 (NB600-254, Novus Biologicals), WDR5 (ab56919; abcam), CYB5R2 (H00051700-B02P; abnova), CYP26B1 (H00056603-M01; abnova), UCP2 (ab97931; abcam) and GAPDH (#5174; Cell signaling).

    Techniques: Expressing

    Identification of HOTTIP target genes. A-B , Expression of HOTTIP target genes ( A ) was inhibited in PDAC cells treated with siHOTTIP; and ( B ) was upregulated in non-tumorigenic human pancreatic ductal epithelial (HPDE) cells when HOTTIP was overexpressed (n=3). C , Expression levels of HOTTIP targets in PDAC FFPE samples, compared to adjacent non-tumor tissues (n=37-47). D , The correlation between CHI3L1, SULT1A1, CLIC5 and HOTTIP expression in PDAC tumor samples. E , Representative images of UCP2 immunohistochemistry on PDAC samples (right panel), compared with adjacent non-tumor tissue (left panel). UCP2 protein level was correlated with HOTTIP expression (lower panel). *P

    Journal: bioRxiv

    Article Title: Ectopic HOTTIP Expression Induces Non-canonical Transactivation Pathways to Promote Growth and Invasiveness in Pancreatic Ductal Adenocarcinoma

    doi: 10.1101/812800

    Figure Lengend Snippet: Identification of HOTTIP target genes. A-B , Expression of HOTTIP target genes ( A ) was inhibited in PDAC cells treated with siHOTTIP; and ( B ) was upregulated in non-tumorigenic human pancreatic ductal epithelial (HPDE) cells when HOTTIP was overexpressed (n=3). C , Expression levels of HOTTIP targets in PDAC FFPE samples, compared to adjacent non-tumor tissues (n=37-47). D , The correlation between CHI3L1, SULT1A1, CLIC5 and HOTTIP expression in PDAC tumor samples. E , Representative images of UCP2 immunohistochemistry on PDAC samples (right panel), compared with adjacent non-tumor tissue (left panel). UCP2 protein level was correlated with HOTTIP expression (lower panel). *P

    Article Snippet: Proteins were separated by SDS-PAGE, transferred to PVDF membrane and immunoblotted overnight at 4 °C with 1:1000 primary antibodies against HOXA13 (ab106503; abcam), MLL1 (#ABE240; Millipore), MLL2 (#ABE206, Millipore), MLL4 (NB600-254, Novus Biologicals), WDR5 (ab56919; abcam), CYB5R2 (H00051700-B02P; abnova), CYP26B1 (H00056603-M01; abnova), UCP2 (ab97931; abcam) and GAPDH (#5174; Cell signaling).

    Techniques: Expressing, Formalin-fixed Paraffin-Embedded, Immunohistochemistry

    High-Fat Diet Induces a Rapid and Transient Upregulation of Ucp2 mRNA Levels and a Rapid and Transient Change in Mitochondrial Morphology A–E) Real-time PCR data showing relative mRNA levels of Ucp2 (A), IL-1β (B), IL-6 (C), Tnfα (D), and Cx3cr1 (E) in isolated hypothalamic microglia (CD11b + cells) from male mice fed on standard chow diet (SD), 3-day high-fat diet (3d HFD), 7-day HFD (7d HFD), or 8-week HFD (8w HFD) (n = 4–6 mice per group). (F) Representative electron micrographs showing mitochondria (asterisks) in microglial cells in the arcuate nucleus of the hypothalamus of male mice exposed to SD, 3d HFD, 7d HFD, or 8w HFD. (G–I) Average mitochondrial area (G), mitochondrial density (H), and mitochondrial coverage (I), in microglial cells from male mice fed on SD (n = 5), 3d HFD (n = 6), 7d HFD (n = 5), or 8w HFD (n = 5). (J) Graph showing the percentage of phosphorylated DRP1 (p-Drp1) at site S616 (activated form) in tomato-positive cells (microglia) in the hypothalamus and cortex of mice exposed to either standard chow diet (SD; n = 3) or 3d HFD (n = 5). .

    Journal: Cell metabolism

    Article Title: Microglial UCP2 Mediates Inflammation and Obesity Induced by High-Fat Feeding

    doi: 10.1016/j.cmet.2019.08.010

    Figure Lengend Snippet: High-Fat Diet Induces a Rapid and Transient Upregulation of Ucp2 mRNA Levels and a Rapid and Transient Change in Mitochondrial Morphology A–E) Real-time PCR data showing relative mRNA levels of Ucp2 (A), IL-1β (B), IL-6 (C), Tnfα (D), and Cx3cr1 (E) in isolated hypothalamic microglia (CD11b + cells) from male mice fed on standard chow diet (SD), 3-day high-fat diet (3d HFD), 7-day HFD (7d HFD), or 8-week HFD (8w HFD) (n = 4–6 mice per group). (F) Representative electron micrographs showing mitochondria (asterisks) in microglial cells in the arcuate nucleus of the hypothalamus of male mice exposed to SD, 3d HFD, 7d HFD, or 8w HFD. (G–I) Average mitochondrial area (G), mitochondrial density (H), and mitochondrial coverage (I), in microglial cells from male mice fed on SD (n = 5), 3d HFD (n = 6), 7d HFD (n = 5), or 8w HFD (n = 5). (J) Graph showing the percentage of phosphorylated DRP1 (p-Drp1) at site S616 (activated form) in tomato-positive cells (microglia) in the hypothalamus and cortex of mice exposed to either standard chow diet (SD; n = 3) or 3d HFD (n = 5). .

    Article Snippet: The following Primers were used: Ucp2, Mm00627599_m1; IL-1β,Mm00434228_m1; IL-6, Mm00446190_m1; Tnf, Mm00443258; IL-10, Mm01288386_m1; Cx3cr1, Mm02620111_s1; Hspa1a (known as Hsp72), Mm01159846_s1; Gfap, Mm01253033_m1; Gapdh, Mm99999915_g1; β-Actin, Mm02619580.

    Techniques: Real-time Polymerase Chain Reaction, Isolation, Mouse Assay

    Selective Deletion of UCP2 in Microglia Affects Mitochondrial Function (A–C) Graphs showing the OCR (A and B) and ECAR (C) under L-glutamine (2 mM) incubation (n = 4 for controls and n = 3 for Ucp2 MGKO mice) in primary microglial cell culture of control and Ucp2 MGKO mice. (D–F) Graphs showing the OCR (D and E) and ECAR (F) under L-glutamine (2 mM) and palmitate (200 μM) incubation (n = 5 for controls and n = 5 for Ucp2 MGKO mice) in primary microglial cell culture of control and Ucp2 MGKO mice. (G–I) Graphs showing the OCR (G and H) and ECAR (I) under L-glutamine (2 mM) and glucose (25 mM) incubation (n = 5 for controls and n = 5 for Ucp2 MGKO mice) in primary microglial cell culture of control and Ucp2 MGKO mice. (J–L) Graphs showing the OCR (J and K) and ECAR (L) under L-glutamine (2 mM), glucose (25 mM), and palmitate (200 μM) incubation (n = 5 for controls and n = 5 for Ucp2 MGKO mice) in primary microglial cell culture of control and Ucp2 MGKO mice. (M–O) Graphs showing basal respiration (M), maximal respiration (N), and ATP production (O) of primary microglial cells from control mice. (P–R) Graphs showing basal respiration (P), maximal respiration (Q), and ATP production (R) of primary microglial cells from Ucp2 MGKO mice. .

    Journal: Cell metabolism

    Article Title: Microglial UCP2 Mediates Inflammation and Obesity Induced by High-Fat Feeding

    doi: 10.1016/j.cmet.2019.08.010

    Figure Lengend Snippet: Selective Deletion of UCP2 in Microglia Affects Mitochondrial Function (A–C) Graphs showing the OCR (A and B) and ECAR (C) under L-glutamine (2 mM) incubation (n = 4 for controls and n = 3 for Ucp2 MGKO mice) in primary microglial cell culture of control and Ucp2 MGKO mice. (D–F) Graphs showing the OCR (D and E) and ECAR (F) under L-glutamine (2 mM) and palmitate (200 μM) incubation (n = 5 for controls and n = 5 for Ucp2 MGKO mice) in primary microglial cell culture of control and Ucp2 MGKO mice. (G–I) Graphs showing the OCR (G and H) and ECAR (I) under L-glutamine (2 mM) and glucose (25 mM) incubation (n = 5 for controls and n = 5 for Ucp2 MGKO mice) in primary microglial cell culture of control and Ucp2 MGKO mice. (J–L) Graphs showing the OCR (J and K) and ECAR (L) under L-glutamine (2 mM), glucose (25 mM), and palmitate (200 μM) incubation (n = 5 for controls and n = 5 for Ucp2 MGKO mice) in primary microglial cell culture of control and Ucp2 MGKO mice. (M–O) Graphs showing basal respiration (M), maximal respiration (N), and ATP production (O) of primary microglial cells from control mice. (P–R) Graphs showing basal respiration (P), maximal respiration (Q), and ATP production (R) of primary microglial cells from Ucp2 MGKO mice. .

    Article Snippet: The following Primers were used: Ucp2, Mm00627599_m1; IL-1β,Mm00434228_m1; IL-6, Mm00446190_m1; Tnf, Mm00443258; IL-10, Mm01288386_m1; Cx3cr1, Mm02620111_s1; Hspa1a (known as Hsp72), Mm01159846_s1; Gfap, Mm01253033_m1; Gapdh, Mm99999915_g1; β-Actin, Mm02619580.

    Techniques: Incubation, Mouse Assay, Cell Culture

    Selective Deletion of UCP2 in Microglia Affects HFD-Induced Microglial Activation A) Representative micrographs of hypothalamic sections showing tomato-expressing microglia in the mediobasal hypothalamus of male control (upper panels) and Ucp2 MGKO mice (lower panels) fed on SD (n = 8 for both groups), 3d HFD (n = 7 for both groups), 7d HFD (n = 8 for controls and n = 7 for Ucp2 MGKO mice), and 8w HFD (n = 8 for controls and n = 7 for Ucp2 MGKO mice). (B) Graph showing the number of microglia in the ARC of control and Ucp2 MGKO mice fed on SD (n = 8 for both groups), 3d HFD (n = 7 for both groups), 7d HFD (n = 8 for controls and n = 7 for Ucp2 MGKO mice), and 8w HFD (n = 8 for controls and n = 7 for Ucp2 MGKO mice). (C) Graph showing microglia size in the ARC of control and of Ucp2 MGKO mice fed on SD (n = 8 for both groups), 3d HFD (n = 7 for both groups), 7d HFD (n = 8 for controls and n = 7 for Ucp2 MGKO mice), and 8w HFD (n = 8 for controls and n = 7 for Ucp2 MGKO mice). (D) Graph showing microglia number in the VMH of control and Ucp2 MGKO mice fed on SD, 3d HFD, 7d HFD, and 8w HFD (n = 5 mice/group). (E) Graph showing microglia size in the VMH of control and Ucp2 MGKO mice fed on SD, 3d HFD, 7d HFD, and 8w HFD (n = 5 mice/group). .

    Journal: Cell metabolism

    Article Title: Microglial UCP2 Mediates Inflammation and Obesity Induced by High-Fat Feeding

    doi: 10.1016/j.cmet.2019.08.010

    Figure Lengend Snippet: Selective Deletion of UCP2 in Microglia Affects HFD-Induced Microglial Activation A) Representative micrographs of hypothalamic sections showing tomato-expressing microglia in the mediobasal hypothalamus of male control (upper panels) and Ucp2 MGKO mice (lower panels) fed on SD (n = 8 for both groups), 3d HFD (n = 7 for both groups), 7d HFD (n = 8 for controls and n = 7 for Ucp2 MGKO mice), and 8w HFD (n = 8 for controls and n = 7 for Ucp2 MGKO mice). (B) Graph showing the number of microglia in the ARC of control and Ucp2 MGKO mice fed on SD (n = 8 for both groups), 3d HFD (n = 7 for both groups), 7d HFD (n = 8 for controls and n = 7 for Ucp2 MGKO mice), and 8w HFD (n = 8 for controls and n = 7 for Ucp2 MGKO mice). (C) Graph showing microglia size in the ARC of control and of Ucp2 MGKO mice fed on SD (n = 8 for both groups), 3d HFD (n = 7 for both groups), 7d HFD (n = 8 for controls and n = 7 for Ucp2 MGKO mice), and 8w HFD (n = 8 for controls and n = 7 for Ucp2 MGKO mice). (D) Graph showing microglia number in the VMH of control and Ucp2 MGKO mice fed on SD, 3d HFD, 7d HFD, and 8w HFD (n = 5 mice/group). (E) Graph showing microglia size in the VMH of control and Ucp2 MGKO mice fed on SD, 3d HFD, 7d HFD, and 8w HFD (n = 5 mice/group). .

    Article Snippet: The following Primers were used: Ucp2, Mm00627599_m1; IL-1β,Mm00434228_m1; IL-6, Mm00446190_m1; Tnf, Mm00443258; IL-10, Mm01288386_m1; Cx3cr1, Mm02620111_s1; Hspa1a (known as Hsp72), Mm01159846_s1; Gfap, Mm01253033_m1; Gapdh, Mm99999915_g1; β-Actin, Mm02619580.

    Techniques: Activation Assay, Expressing, Mouse Assay

    Selective Deletion of UCP2 Prevents HFD-Induced Mitochondrial Dynamics (A) Representative electron microscopic pictures showing mitochondria (asterisks) in microglia cells of male Ucp2 MGKO mice fed on SD, 3d HFD, 7d HFD, or 8w HFD. (B–D) Average mitochondrial area (B), mitochondrial density (C), and mitochondrial coverage (D) in microglial cells of Ucp2 MGKO mice fed on SD (n = 4), 3d HFD (n = 6), 7d HFD (n = 6), or 8w HFD (n = 5). (E) Graph showing the percentage of phosphorylated DRP1 at site S616 (activated form) in tomato-positive cells (microglia) in the hypothalamus and cortex of male Ucp2 MGKO mice exposed to either SD (n = 3) or 3d HFD (n = 5). .

    Journal: Cell metabolism

    Article Title: Microglial UCP2 Mediates Inflammation and Obesity Induced by High-Fat Feeding

    doi: 10.1016/j.cmet.2019.08.010

    Figure Lengend Snippet: Selective Deletion of UCP2 Prevents HFD-Induced Mitochondrial Dynamics (A) Representative electron microscopic pictures showing mitochondria (asterisks) in microglia cells of male Ucp2 MGKO mice fed on SD, 3d HFD, 7d HFD, or 8w HFD. (B–D) Average mitochondrial area (B), mitochondrial density (C), and mitochondrial coverage (D) in microglial cells of Ucp2 MGKO mice fed on SD (n = 4), 3d HFD (n = 6), 7d HFD (n = 6), or 8w HFD (n = 5). (E) Graph showing the percentage of phosphorylated DRP1 at site S616 (activated form) in tomato-positive cells (microglia) in the hypothalamus and cortex of male Ucp2 MGKO mice exposed to either SD (n = 3) or 3d HFD (n = 5). .

    Article Snippet: The following Primers were used: Ucp2, Mm00627599_m1; IL-1β,Mm00434228_m1; IL-6, Mm00446190_m1; Tnf, Mm00443258; IL-10, Mm01288386_m1; Cx3cr1, Mm02620111_s1; Hspa1a (known as Hsp72), Mm01159846_s1; Gfap, Mm01253033_m1; Gapdh, Mm99999915_g1; β-Actin, Mm02619580.

    Techniques: Mouse Assay

    Validation of the Animal Model A) Graph showing Ucp2 mRNA levels in isolated hypothalamic microglia (CD11b-positive cells, CD11b + ) of male control (n = 4) and Ucp2 MGKO mice (n = 4). (B) Graph showing Ucp2 mRNA levels in isolated hypothalamic CD11b-negative (CD11b − ) cells of control (n = 4) and Ucp2 MGKO mice (n = 4). (C) Graph showing Cx3cr1 mRNA levels in isolated hypothalamic CD11b + and CD11b − cells of control (n = 4) and Ucp2 MGKO mice (n = 4) showing marginal expression of Cx3cr1 mRNA expression in CD11b − cells. (D) Graph showing Ucp2 mRNA levels in peripheral CD11b + cells of the liver, spleen, blood, and brown adipose tissue (BAT) in control (n = 4) and Ucp2 MGKO mice (n = 4). (E) Graphs showing Cx3cr1 mRNA levels in isolated peripheral CD11b + and CD11b − cells of control mice (n = 4). Note the not detectable (ND) or marginal (in spleen) expression of Cx3cr1 mRNA expression in CD11b − cells as validation of the data shown in (D). .

    Journal: Cell metabolism

    Article Title: Microglial UCP2 Mediates Inflammation and Obesity Induced by High-Fat Feeding

    doi: 10.1016/j.cmet.2019.08.010

    Figure Lengend Snippet: Validation of the Animal Model A) Graph showing Ucp2 mRNA levels in isolated hypothalamic microglia (CD11b-positive cells, CD11b + ) of male control (n = 4) and Ucp2 MGKO mice (n = 4). (B) Graph showing Ucp2 mRNA levels in isolated hypothalamic CD11b-negative (CD11b − ) cells of control (n = 4) and Ucp2 MGKO mice (n = 4). (C) Graph showing Cx3cr1 mRNA levels in isolated hypothalamic CD11b + and CD11b − cells of control (n = 4) and Ucp2 MGKO mice (n = 4) showing marginal expression of Cx3cr1 mRNA expression in CD11b − cells. (D) Graph showing Ucp2 mRNA levels in peripheral CD11b + cells of the liver, spleen, blood, and brown adipose tissue (BAT) in control (n = 4) and Ucp2 MGKO mice (n = 4). (E) Graphs showing Cx3cr1 mRNA levels in isolated peripheral CD11b + and CD11b − cells of control mice (n = 4). Note the not detectable (ND) or marginal (in spleen) expression of Cx3cr1 mRNA expression in CD11b − cells as validation of the data shown in (D). .

    Article Snippet: The following Primers were used: Ucp2, Mm00627599_m1; IL-1β,Mm00434228_m1; IL-6, Mm00446190_m1; Tnf, Mm00443258; IL-10, Mm01288386_m1; Cx3cr1, Mm02620111_s1; Hspa1a (known as Hsp72), Mm01159846_s1; Gfap, Mm01253033_m1; Gapdh, Mm99999915_g1; β-Actin, Mm02619580.

    Techniques: Animal Model, Isolation, Mouse Assay, Expressing

    Selective Deletion of UCP2 in Microglia Affects POMC Synaptic Input Organization and Neuronal Activation (A) Graphs showing the total number of synapses onto POMC neurons of male SD-fed controls (11 cells/3 mice), 8w HFD-fed controls (14 cells/3 mice), SD-fed Ucp2 MGKO mice (19 cells/4 mice), and 8w HFD-fed Ucp2 MGKO mice (17 cells/4 mice for HFD). (B) Graphs showing the number of asymmetrical (putative excitatory) synapses onto POMC neurons of male SD-fed controls (11 cells/3 mice), 8w HFD-fed controls (14 cells/3 mice), SD-fed Ucp2 MGKO mice (19 cells/4 mice), and 8w HFD-fed Ucp2 MGKO mice (17 cells/4 mice for HFD). (C) Graphs showing the number of symmetrical (putative inhibitory) synapses onto POMC neurons of male SD-fed controls (11 cells/3 mice), 8w HFD-fed controls (14 cells/3 mice), SD-fed Ucp2 MGKO mice (19 cells/4 mice), and 8w HFD-fed Ucp2 MGKO mice (17 cells/4 mice for HFD). (D and E) Representative electron micrographs showing examples of asymmetrical (D) and symmetrical (E) synapses onto POMC neurons. Arrowheads in (D) indicate postsynaptic density characteristic of asymmetrical excitatory synapsis. Asterisks indicate axon terminals. (F) Representative micrographs showing hypothalamic sections of fed male control (upper panels) and Ucp2 MGKO mice (lower panels) on HFD immunostained for POMC (left panels in green), c-Fos (middle panels in red), and merged (right panels). (G) Graph showing the percentage of c-Fos-positive POMC neurons in fed male control and Ucp2 MGKO mice (n = 4 for both groups) on HFD. (H) Graph showing no difference in total POMC cell number in fed male control and Ucp2 MGKO mice (n = 4 for both groups) on HFD. . 3v, 3 rd ventricle; ARC, arcuate nucleus; ME, median eminence.

    Journal: Cell metabolism

    Article Title: Microglial UCP2 Mediates Inflammation and Obesity Induced by High-Fat Feeding

    doi: 10.1016/j.cmet.2019.08.010

    Figure Lengend Snippet: Selective Deletion of UCP2 in Microglia Affects POMC Synaptic Input Organization and Neuronal Activation (A) Graphs showing the total number of synapses onto POMC neurons of male SD-fed controls (11 cells/3 mice), 8w HFD-fed controls (14 cells/3 mice), SD-fed Ucp2 MGKO mice (19 cells/4 mice), and 8w HFD-fed Ucp2 MGKO mice (17 cells/4 mice for HFD). (B) Graphs showing the number of asymmetrical (putative excitatory) synapses onto POMC neurons of male SD-fed controls (11 cells/3 mice), 8w HFD-fed controls (14 cells/3 mice), SD-fed Ucp2 MGKO mice (19 cells/4 mice), and 8w HFD-fed Ucp2 MGKO mice (17 cells/4 mice for HFD). (C) Graphs showing the number of symmetrical (putative inhibitory) synapses onto POMC neurons of male SD-fed controls (11 cells/3 mice), 8w HFD-fed controls (14 cells/3 mice), SD-fed Ucp2 MGKO mice (19 cells/4 mice), and 8w HFD-fed Ucp2 MGKO mice (17 cells/4 mice for HFD). (D and E) Representative electron micrographs showing examples of asymmetrical (D) and symmetrical (E) synapses onto POMC neurons. Arrowheads in (D) indicate postsynaptic density characteristic of asymmetrical excitatory synapsis. Asterisks indicate axon terminals. (F) Representative micrographs showing hypothalamic sections of fed male control (upper panels) and Ucp2 MGKO mice (lower panels) on HFD immunostained for POMC (left panels in green), c-Fos (middle panels in red), and merged (right panels). (G) Graph showing the percentage of c-Fos-positive POMC neurons in fed male control and Ucp2 MGKO mice (n = 4 for both groups) on HFD. (H) Graph showing no difference in total POMC cell number in fed male control and Ucp2 MGKO mice (n = 4 for both groups) on HFD. . 3v, 3 rd ventricle; ARC, arcuate nucleus; ME, median eminence.

    Article Snippet: The following Primers were used: Ucp2, Mm00627599_m1; IL-1β,Mm00434228_m1; IL-6, Mm00446190_m1; Tnf, Mm00443258; IL-10, Mm01288386_m1; Cx3cr1, Mm02620111_s1; Hspa1a (known as Hsp72), Mm01159846_s1; Gfap, Mm01253033_m1; Gapdh, Mm99999915_g1; β-Actin, Mm02619580.

    Techniques: Activation Assay, Mouse Assay

    Selective Deletion of UCP2 Prevents HFD-Induced Obesity in Male Mice A) Graph showing body weight in male control (n = 8) and Ucp2 MGKO mice (n = 8) fed on HFD for up to 8 weeks. (B and C) Graphs showing fat mass (B) and lean mass (C) in male control and Ucp2 MGKO mice on HFD for 4 weeks. (D–L) Graphs showing energy expenditure (D–F), consumed O 2 (G and H), produced CO 2 (I and J), and the respiratory exchange ratio (RER) (K and L) in male control and Ucp2 MGKO mice on HFD for 4 weeks. (M and N) Graphs showing 24 h food intake (M; average of 3 days) and 48 h locomotor activity (N) of male control and Ucp2 MGKO mice on HFD for 4 weeks. (O and P) Graphs showing glucose tolerance test (O) and insulin tolerance test (P) of male control and Ucp2 MGKO mice on HFD for 4 weeks. .

    Journal: Cell metabolism

    Article Title: Microglial UCP2 Mediates Inflammation and Obesity Induced by High-Fat Feeding

    doi: 10.1016/j.cmet.2019.08.010

    Figure Lengend Snippet: Selective Deletion of UCP2 Prevents HFD-Induced Obesity in Male Mice A) Graph showing body weight in male control (n = 8) and Ucp2 MGKO mice (n = 8) fed on HFD for up to 8 weeks. (B and C) Graphs showing fat mass (B) and lean mass (C) in male control and Ucp2 MGKO mice on HFD for 4 weeks. (D–L) Graphs showing energy expenditure (D–F), consumed O 2 (G and H), produced CO 2 (I and J), and the respiratory exchange ratio (RER) (K and L) in male control and Ucp2 MGKO mice on HFD for 4 weeks. (M and N) Graphs showing 24 h food intake (M; average of 3 days) and 48 h locomotor activity (N) of male control and Ucp2 MGKO mice on HFD for 4 weeks. (O and P) Graphs showing glucose tolerance test (O) and insulin tolerance test (P) of male control and Ucp2 MGKO mice on HFD for 4 weeks. .

    Article Snippet: The following Primers were used: Ucp2, Mm00627599_m1; IL-1β,Mm00434228_m1; IL-6, Mm00446190_m1; Tnf, Mm00443258; IL-10, Mm01288386_m1; Cx3cr1, Mm02620111_s1; Hspa1a (known as Hsp72), Mm01159846_s1; Gfap, Mm01253033_m1; Gapdh, Mm99999915_g1; β-Actin, Mm02619580.

    Techniques: Mouse Assay, Produced, Activity Assay

    Effects of 100 μM 1-monooleyl glycerol (1-MOG) and 2-monooley glycerol (2-MOG) on expression of mRNA of acyl-CoA oxidase (ACO)  A ) medium-chain acyl-CoA dehydrogenase (MCAD)  B ) fatty acid translocase (FAT)  C ) and uncoupling protein-2 (UCP-2)  D ) in the Caco-2 cells. Notes:  Boxes and bars indicate mean ± SD of relative quantitation mRNA values using 18S as an internal control. N = 8. * P

    Journal: Diabetes, metabolic syndrome and obesity : targets and therapy

    Article Title: A molecular mechanism for diacylglycerol-mediated promotion of negative caloric balance

    doi:

    Figure Lengend Snippet: Effects of 100 μM 1-monooleyl glycerol (1-MOG) and 2-monooley glycerol (2-MOG) on expression of mRNA of acyl-CoA oxidase (ACO) A ) medium-chain acyl-CoA dehydrogenase (MCAD) B ) fatty acid translocase (FAT) C ) and uncoupling protein-2 (UCP-2) D ) in the Caco-2 cells. Notes: Boxes and bars indicate mean ± SD of relative quantitation mRNA values using 18S as an internal control. N = 8. * P

    Article Snippet: The Taqman Gene Expression Assays Hs01074241, Hs00936576, Hs01567186, Hs01075227, and Hs99999901_S1 were used for ACO, MCAD, FAT, UCP-2, and 18S, respectively.

    Techniques: Expressing, Quantitation Assay

    The relative gene expression of SREBP1 ( Srebf1 ), PPAR‐alpha ( Ppara ), DGAT‐1 ( Dgat1 ), FAS ( Fasn ) and ACC1 ( Acaca ) in the liver (A) and SREBP1 ( Srebf1 ), PPAR‐alpha ( Ppara ), DGAT‐1 ( Dgat1 ), UCP2 ( Ucp2 ) and HSL ( Lipe ) in the adipose tissue (B) with regard to SKL‐14959 treatment. Values are expressed as means ± standard deviation (eight to nine mice per group). # p

    Journal: Obesity Science & Practice

    Article Title: Gastric inhibitory polypeptide receptor antagonist, SKL‐14959, suppressed body weight gain on diet‐induced obesity mice) Gastric inhibitory polypeptide receptor antagonist, SKL‐14959, suppressed body weight gain on diet‐induced obesity mice

    doi: 10.1002/osp4.164

    Figure Lengend Snippet: The relative gene expression of SREBP1 ( Srebf1 ), PPAR‐alpha ( Ppara ), DGAT‐1 ( Dgat1 ), FAS ( Fasn ) and ACC1 ( Acaca ) in the liver (A) and SREBP1 ( Srebf1 ), PPAR‐alpha ( Ppara ), DGAT‐1 ( Dgat1 ), UCP2 ( Ucp2 ) and HSL ( Lipe ) in the adipose tissue (B) with regard to SKL‐14959 treatment. Values are expressed as means ± standard deviation (eight to nine mice per group). # p

    Article Snippet: Polymerase chain reactions for each target cDNA were carried out using commercially supplied ready‐to use primer and probe sets by Applied Biosystems (TaqMan gene expression assays): sterol regulatory element binding transcription factor 1, Srebf1 (Mm00550338_m1), diacylglycerol O‐acyltransferase 1, Dgat1 (Mm00515643_m1), fatty acid synthase, Fasn (Mm01253292_m1), acetyl‐coenzyme A carboxylase alpha, Acaca (Mm01304257_m1), peroxisome proliferator activated receptor alpha, Ppara (Mm00440939_m1), uncoupling protein 2, Ucp2 (Mm00627598_m1), hormone sensitive lipase, Lipe (Mm00495359_m1) and TATA box binding protein, TBP (Mm0111222) as housekeeping gene.

    Techniques: Expressing, Standard Deviation, Mouse Assay

    UCP2 decreases mast cell histidine decarboxylase expression

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: The mitochondrial uncoupling protein 2 (UCP2) inhibits mast cell activation and reduces histamine content †

    doi: 10.4049/jimmunol.0803422

    Figure Lengend Snippet: UCP2 decreases mast cell histidine decarboxylase expression

    Article Snippet: After blocking with 5% milk, membranes were probed overnight at 4°C with either goat anti-UCP2 (1:400, Santa Cruz) or rabbit anti-histidine decarboxylase (1:300, Abcam, Cambridge, MA).

    Techniques: Expressing

    Enhanced vascular permeability in Ucp2 −/− mouse skin

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: The mitochondrial uncoupling protein 2 (UCP2) inhibits mast cell activation and reduces histamine content †

    doi: 10.4049/jimmunol.0803422

    Figure Lengend Snippet: Enhanced vascular permeability in Ucp2 −/− mouse skin

    Article Snippet: After blocking with 5% milk, membranes were probed overnight at 4°C with either goat anti-UCP2 (1:400, Santa Cruz) or rabbit anti-histidine decarboxylase (1:300, Abcam, Cambridge, MA).

    Techniques: Permeability

    Ucp2 −/− BMMCs have augmented PGD 2 release and ERK activation

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: The mitochondrial uncoupling protein 2 (UCP2) inhibits mast cell activation and reduces histamine content †

    doi: 10.4049/jimmunol.0803422

    Figure Lengend Snippet: Ucp2 −/− BMMCs have augmented PGD 2 release and ERK activation

    Article Snippet: After blocking with 5% milk, membranes were probed overnight at 4°C with either goat anti-UCP2 (1:400, Santa Cruz) or rabbit anti-histidine decarboxylase (1:300, Abcam, Cambridge, MA).

    Techniques: Activation Assay

    UCP2-deficient mast cells have enhanced degranulation

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: The mitochondrial uncoupling protein 2 (UCP2) inhibits mast cell activation and reduces histamine content †

    doi: 10.4049/jimmunol.0803422

    Figure Lengend Snippet: UCP2-deficient mast cells have enhanced degranulation

    Article Snippet: After blocking with 5% milk, membranes were probed overnight at 4°C with either goat anti-UCP2 (1:400, Santa Cruz) or rabbit anti-histidine decarboxylase (1:300, Abcam, Cambridge, MA).

    Techniques:

    Overexpression of UCP2 in LAD2 cells inhibits histamine release

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: The mitochondrial uncoupling protein 2 (UCP2) inhibits mast cell activation and reduces histamine content †

    doi: 10.4049/jimmunol.0803422

    Figure Lengend Snippet: Overexpression of UCP2 in LAD2 cells inhibits histamine release

    Article Snippet: After blocking with 5% milk, membranes were probed overnight at 4°C with either goat anti-UCP2 (1:400, Santa Cruz) or rabbit anti-histidine decarboxylase (1:300, Abcam, Cambridge, MA).

    Techniques: Over Expression

    UCP2 decreases mast cell histamine content

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: The mitochondrial uncoupling protein 2 (UCP2) inhibits mast cell activation and reduces histamine content †

    doi: 10.4049/jimmunol.0803422

    Figure Lengend Snippet: UCP2 decreases mast cell histamine content

    Article Snippet: After blocking with 5% milk, membranes were probed overnight at 4°C with either goat anti-UCP2 (1:400, Santa Cruz) or rabbit anti-histidine decarboxylase (1:300, Abcam, Cambridge, MA).

    Techniques:

    Ucp2 −/− BMMC have augmented IL-6 release

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: The mitochondrial uncoupling protein 2 (UCP2) inhibits mast cell activation and reduces histamine content †

    doi: 10.4049/jimmunol.0803422

    Figure Lengend Snippet: Ucp2 −/− BMMC have augmented IL-6 release

    Article Snippet: After blocking with 5% milk, membranes were probed overnight at 4°C with either goat anti-UCP2 (1:400, Santa Cruz) or rabbit anti-histidine decarboxylase (1:300, Abcam, Cambridge, MA).

    Techniques:

    UCP2 is expressed in mouse and human mast cells

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: The mitochondrial uncoupling protein 2 (UCP2) inhibits mast cell activation and reduces histamine content †

    doi: 10.4049/jimmunol.0803422

    Figure Lengend Snippet: UCP2 is expressed in mouse and human mast cells

    Article Snippet: After blocking with 5% milk, membranes were probed overnight at 4°C with either goat anti-UCP2 (1:400, Santa Cruz) or rabbit anti-histidine decarboxylase (1:300, Abcam, Cambridge, MA).

    Techniques:

    Uncoupling protein 2 (UCP2) expression induces cell death. (A) Trypan Blue count. Viability of transfected cells: 3% in Lipofectamine and noncoding and vector-transfected cells, 11% in sense UCP2-transfected cells. (B) Live staining with Annexin-V in

    Journal: Metabolic Syndrome and Related Disorders

    Article Title: Mitochondrial Uncoupling Protein 2 Induces Cell Cycle Arrest and Necrotic Cell Death

    doi: 10.1089/met.2013.0096

    Figure Lengend Snippet: Uncoupling protein 2 (UCP2) expression induces cell death. (A) Trypan Blue count. Viability of transfected cells: 3% in Lipofectamine and noncoding and vector-transfected cells, 11% in sense UCP2-transfected cells. (B) Live staining with Annexin-V in

    Article Snippet: Immunostaining was performed with goat anti-UCP2 antibody (Santa Cruz, 1:200 dilution in PBS containing 1% BSA and 0.05% Triton-100) and then TRITC-labeled rabbit anti-goat antibody (Sigma).

    Techniques: Expressing, Transfection, Plasmid Preparation, Staining

    Overexpression of UCP2 inhibits cell division

    Journal: Metabolic Syndrome and Related Disorders

    Article Title: Mitochondrial Uncoupling Protein 2 Induces Cell Cycle Arrest and Necrotic Cell Death

    doi: 10.1089/met.2013.0096

    Figure Lengend Snippet: Overexpression of UCP2 inhibits cell division

    Article Snippet: Immunostaining was performed with goat anti-UCP2 antibody (Santa Cruz, 1:200 dilution in PBS containing 1% BSA and 0.05% Triton-100) and then TRITC-labeled rabbit anti-goat antibody (Sigma).

    Techniques: Over Expression

    Un c oupling protein 2 (UCP2) expression has minimal effect on intracellular adenosine triphosphate (ATP) content (A) , but slightly increases glutathione (GSH) contents (B) in transfected cells. From left to right: transfection with C-UCP2, N-UCP2, noncoding-UCP2,

    Journal: Metabolic Syndrome and Related Disorders

    Article Title: Mitochondrial Uncoupling Protein 2 Induces Cell Cycle Arrest and Necrotic Cell Death

    doi: 10.1089/met.2013.0096

    Figure Lengend Snippet: Un c oupling protein 2 (UCP2) expression has minimal effect on intracellular adenosine triphosphate (ATP) content (A) , but slightly increases glutathione (GSH) contents (B) in transfected cells. From left to right: transfection with C-UCP2, N-UCP2, noncoding-UCP2,

    Article Snippet: Immunostaining was performed with goat anti-UCP2 antibody (Santa Cruz, 1:200 dilution in PBS containing 1% BSA and 0.05% Triton-100) and then TRITC-labeled rabbit anti-goat antibody (Sigma).

    Techniques: Expressing, Transfection

    Expression patterns of the uncoupling protein 2 (UCP2) fusion protein in Hepa 1–6 cells. (A) Green fluorescent protein (GFP) and fluorescent UCP2 immunocytochemistry (IC) signals of Hepa 1–6 cells transfected with either C-sense UCP2 or

    Journal: Metabolic Syndrome and Related Disorders

    Article Title: Mitochondrial Uncoupling Protein 2 Induces Cell Cycle Arrest and Necrotic Cell Death

    doi: 10.1089/met.2013.0096

    Figure Lengend Snippet: Expression patterns of the uncoupling protein 2 (UCP2) fusion protein in Hepa 1–6 cells. (A) Green fluorescent protein (GFP) and fluorescent UCP2 immunocytochemistry (IC) signals of Hepa 1–6 cells transfected with either C-sense UCP2 or

    Article Snippet: Immunostaining was performed with goat anti-UCP2 antibody (Santa Cruz, 1:200 dilution in PBS containing 1% BSA and 0.05% Triton-100) and then TRITC-labeled rabbit anti-goat antibody (Sigma).

    Techniques: Expressing, Immunocytochemistry, Transfection

    Uncoupling protein 2 (UCP2) expression inhibits cell proliferation with G 1 phase arrest in Hepa 1–6 cells. This figure shows cell cycle analysis of UCP2-transfected Hepa 1–6 cells by flow cytometry, comparing cell cycle patterns of green

    Journal: Metabolic Syndrome and Related Disorders

    Article Title: Mitochondrial Uncoupling Protein 2 Induces Cell Cycle Arrest and Necrotic Cell Death

    doi: 10.1089/met.2013.0096

    Figure Lengend Snippet: Uncoupling protein 2 (UCP2) expression inhibits cell proliferation with G 1 phase arrest in Hepa 1–6 cells. This figure shows cell cycle analysis of UCP2-transfected Hepa 1–6 cells by flow cytometry, comparing cell cycle patterns of green

    Article Snippet: Immunostaining was performed with goat anti-UCP2 antibody (Santa Cruz, 1:200 dilution in PBS containing 1% BSA and 0.05% Triton-100) and then TRITC-labeled rabbit anti-goat antibody (Sigma).

    Techniques: Expressing, Cell Cycle Assay, Transfection, Flow Cytometry, Cytometry

    A set of ROS regulating enzymes is coordinately controlled by PPARγ activation. Karpas 299 and SUP-M2 cells treated with 2 μmol/L rosiglitazone or DMSO were harvested at 42 hours after serum withdrawal. A: p67 mRNA was measured by real-time RT-PCR (left). The amount of p67 mRNA in DMSO-treated Karpas 299 cells was arbitrarily set as 100%. p67 protein levels were determined by Western blot analysis in whole-cell lysates (right). D, DMSO; R, rosiglitazone. B: UCP2 mRNA was measured by real-time RT-PCR (left). The amount of UCP2 mRNA in DMSO-treated Karpas 299 cells was arbitrarily set as 100%. UCP2 protein levels were determined by Western blot analysis in whole cell lysates (right). D, DMSO; R, rosiglitazone. C: Mn-SOD mRNA was measured by real-time RT-PCR (left). The amount of Mn-SOD mRNA in DMSO-treated Karpas 299 cells was arbitrarily set as 100%. Mn-SOD activity was determined in whole-cell lysates. D: CuZn-SOD and catalase mRNA levels were determined by real-time RT-PCR. The amount of mRNA in DMSO-treated Karpas 299 cells was arbitrarily set as 100%. Data shown in A–D are mean ± SE of at least three independent experiments.

    Journal: The American Journal of Pathology

    Article Title: Activation of Peroxisome Proliferator-Activated Receptor ? Contributes to the Survival of T Lymphoma Cells by Affecting Cellular Metabolism

    doi: 10.2353/ajpath.2007.060651

    Figure Lengend Snippet: A set of ROS regulating enzymes is coordinately controlled by PPARγ activation. Karpas 299 and SUP-M2 cells treated with 2 μmol/L rosiglitazone or DMSO were harvested at 42 hours after serum withdrawal. A: p67 mRNA was measured by real-time RT-PCR (left). The amount of p67 mRNA in DMSO-treated Karpas 299 cells was arbitrarily set as 100%. p67 protein levels were determined by Western blot analysis in whole-cell lysates (right). D, DMSO; R, rosiglitazone. B: UCP2 mRNA was measured by real-time RT-PCR (left). The amount of UCP2 mRNA in DMSO-treated Karpas 299 cells was arbitrarily set as 100%. UCP2 protein levels were determined by Western blot analysis in whole cell lysates (right). D, DMSO; R, rosiglitazone. C: Mn-SOD mRNA was measured by real-time RT-PCR (left). The amount of Mn-SOD mRNA in DMSO-treated Karpas 299 cells was arbitrarily set as 100%. Mn-SOD activity was determined in whole-cell lysates. D: CuZn-SOD and catalase mRNA levels were determined by real-time RT-PCR. The amount of mRNA in DMSO-treated Karpas 299 cells was arbitrarily set as 100%. Data shown in A–D are mean ± SE of at least three independent experiments.

    Article Snippet: Primers and probe were purchased from ABI for detection of PPARγ (Hs00234592_m1), catalase (Hs00156308_m1), Cu, Zn superoxide dismutase (CuZn-SOD, Hs00166575_m1), p67 (Hs00166416_m1), and UCP2 (Hs00163349_m1); sequences are not provided by the manufacturer.

    Techniques: Activation Assay, Quantitative RT-PCR, Western Blot, Activity Assay

    AMPK activation does not cause a miR-122 down-regulation. A , Mice were treated with metformin (250 mg/kg, ip. ) twice a day at a 12 h-interval for 3 days or 5 days and were sacrificed 12 h after the final treatment. Activated and total AMPK levels in the liver of mice were determined by Western blot analysis using anti-phospho-AMPKα (Thr 172) and AMPKα specific antibodies, respectively (the top panel). Levels of phospho-AMPKα was normalized with respective AMPKα and are illustrated as the % of control group (the second panel). UCP2 mRNA (the third panel) and miR-122 (the last panel) levels were determined by the quantitative RT-PCR, were normalized with β-actin and the U6 snRNA, respectively, and are illustrated as the % of control group. *, p

    Journal: PLoS ONE

    Article Title: MicroRNA-122 Down-Regulation Is Involved in Phenobarbital-Mediated Activation of the Constitutive Androstane Receptor

    doi: 10.1371/journal.pone.0041291

    Figure Lengend Snippet: AMPK activation does not cause a miR-122 down-regulation. A , Mice were treated with metformin (250 mg/kg, ip. ) twice a day at a 12 h-interval for 3 days or 5 days and were sacrificed 12 h after the final treatment. Activated and total AMPK levels in the liver of mice were determined by Western blot analysis using anti-phospho-AMPKα (Thr 172) and AMPKα specific antibodies, respectively (the top panel). Levels of phospho-AMPKα was normalized with respective AMPKα and are illustrated as the % of control group (the second panel). UCP2 mRNA (the third panel) and miR-122 (the last panel) levels were determined by the quantitative RT-PCR, were normalized with β-actin and the U6 snRNA, respectively, and are illustrated as the % of control group. *, p

    Article Snippet: Assay ID of the probes used in this study were as follows: mouse UCP2, Mm00627597_m1; human CUX1, Hs00738851_m1; mouse actin, Mm00607939_s1; human actin:Hs99999903_m1.

    Techniques: Activation Assay, Mouse Assay, Western Blot, Quantitative RT-PCR