peg catalase (Millipore)

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Catalase polyethylene glycol

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Pulmonary artery endothelial cells treated with PEG-catalase showed effective inhibition of 20- HETE (hydroxyeicosatetraenoic acid)-induced increase in fluorescence. However, the experiment excludes potential nonspecific fluorescence of DCF (dichlorofluorescein). This experiment studied the effect of 20-HETE on superoxide production and NADPH oxidase activation.

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Millipore peg catalase

Meant ± SEM values (n =5–6) for ET-1 responses of afferent arterioles from control mice in the absence (black diamonds with black line) or presence of <t>PEG-SOD</t> (200 units mL −1 ) (A) or PEG-catalase (1000 units mL −1 ) (B) or <t>Sulindac</t> (40 mg·kg −1 day −1 for 4 weeks) (C) (blue triangles with blue line), diabetic mice in the absence (grey squares with grey line) or presence of PEG-SOD (A) or PEG catalase (B) or Sulindac) (C) (red crosses with red line). Data are shown for changes in luminal dimeters of afferent arterioles in response to ET-1 (10 −12 - 10 −8 mol·l −1 ). ANOVA, analysis of variance; ET-1, endotheline-1; PEG, polyethylene glycol; SOD, superoxide dismutase; DM, diabetes mellitus.

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1) Product Images from "Enhanced Renal Afferent Arteriolar Reactive Oxygen Species and Contractility to Endothelin-1 Are Associated with Canonical Wnt Signaling in Diabetic Mice"

Article Title: Enhanced Renal Afferent Arteriolar Reactive Oxygen Species and Contractility to Endothelin-1 Are Associated with Canonical Wnt Signaling in Diabetic Mice

Journal: Kidney & blood pressure research

doi: 10.1159/000490334

Meant ± SEM values (n =5–6) for ET-1 responses of afferent arterioles from control mice in the absence (black diamonds with black line) or presence of PEG-SOD (200 units mL −1 ) (A) or PEG-catalase (1000 units mL −1 ) (B) or Sulindac (40 mg·kg −1 day −1 for 4 weeks) (C) (blue triangles with blue line), diabetic mice in the absence (grey squares with grey line) or presence of PEG-SOD (A) or PEG catalase (B) or Sulindac) (C) (red crosses with red line). Data are shown for changes in luminal dimeters of afferent arterioles in response to ET-1 (10 −12 - 10 −8 mol·l −1 ). ANOVA, analysis of variance; ET-1, endotheline-1; PEG, polyethylene glycol; SOD, superoxide dismutase; DM, diabetes mellitus.

Figure Legend Snippet: Meant ± SEM values (n =5–6) for ET-1 responses of afferent arterioles from control mice in the absence (black diamonds with black line) or presence of PEG-SOD (200 units mL −1 ) (A) or PEG-catalase (1000 units mL −1 ) (B) or Sulindac (40 mg·kg −1 day −1 for 4 weeks) (C) (blue triangles with blue line), diabetic mice in the absence (grey squares with grey line) or presence of PEG-SOD (A) or PEG catalase (B) or Sulindac) (C) (red crosses with red line). Data are shown for changes in luminal dimeters of afferent arterioles in response to ET-1 (10 −12 - 10 −8 mol·l −1 ). ANOVA, analysis of variance; ET-1, endotheline-1; PEG, polyethylene glycol; SOD, superoxide dismutase; DM, diabetes mellitus.

Techniques Used: Mouse Assay

2) Product Images from "Restoration of afferent arteriolar autoregulatory behavior in ischemia-reperfusion injury in rat kidneys"

Article Title: Restoration of afferent arteriolar autoregulatory behavior in ischemia-reperfusion injury in rat kidneys

Journal: American Journal of Physiology - Renal Physiology

doi: 10.1152/ajprenal.00500.2020

Acute polyethylene glycol-conjugated superoxide dismutase (PEG-SOD) treatment improved autoregulatory behavior of afferent arterioles in ischemia-reperfused (IR) rats. A : the afferent arteriolar response to alterations in renal perfusion pressure was measured in male sham (circles, n = 7), IR (squares, n = 8), or IR + PEG-SOD (diamonds, n = 6) rats. PEG-SOD (100 U/mL) was delivered in the reconstituted perfusate blood, and the kidney was perfused for 20–25 min before the autoregulatory protocol was started. B : data were normalized as a percentage of the baseline diameter at 100 mmHg. Values are means ± SE. For within-group analysis, one-way repeated-measures ANOVA with a Dunnett’s post hoc test was performed. * P

Figure Legend Snippet: Acute polyethylene glycol-conjugated superoxide dismutase (PEG-SOD) treatment improved autoregulatory behavior of afferent arterioles in ischemia-reperfused (IR) rats. A : the afferent arteriolar response to alterations in renal perfusion pressure was measured in male sham (circles, n = 7), IR (squares, n = 8), or IR + PEG-SOD (diamonds, n = 6) rats. PEG-SOD (100 U/mL) was delivered in the reconstituted perfusate blood, and the kidney was perfused for 20–25 min before the autoregulatory protocol was started. B : data were normalized as a percentage of the baseline diameter at 100 mmHg. Values are means ± SE. For within-group analysis, one-way repeated-measures ANOVA with a Dunnett’s post hoc test was performed. * P

Techniques Used:

Figure Legend Snippet: Acute polyethylene glycol-conjugated superoxide dismutase (PEG-SOD) or polyethylene glycol-conjugated catalase (PEG-catalase) treatment did not alter afferent arteriolar autoregulatory profile in sham rats. A : the afferent arteriolar response to alterations in renal perfusion pressure was measured in male sham (circles, n = 7), sham + PEG-SOD (squares, n = 6), or sham + PEG-catalase (diamonds, n = 5) rats. PEG-SOD (100 U/mL) or PEG-catalase (1,000 U/mL) was delivered in the reconstituted perfusate blood, and the kidney was perfused for 20–25 min before the autoregulatory protocol was started. B : data were normalized as a percentage of the baseline diameter at 100 mmHg. Values are means ± SE. For within-group analysis, one-way repeated-measures ANOVA with a Dunnett’s post hoc test was performed. * P

Techniques Used:

3) Product Images from "ÃÂ±1AMPK deletion in myelomonocytic cells induces a pro-inflammatory phenotype and enhances angiotensin II-induced vascular dysfunction"

Article Title: ÃÂ±1AMPK deletion in myelomonocytic cells induces a pro-inflammatory phenotype and enhances angiotensin II-induced vascular dysfunction

Journal: Cardiovascular Research

doi: 10.1093/cvr/cvy172

Vascular oxidative stress is increased in mice lacking myelomonocytic cell α1AMPK. ( A ) Aortic 3-nitrotyrosine staining was used as a surrogate for peroxynitrite formation and assessed by dot blot technique. Pooled samples ( n = 3) of n = 6 mice. ( B ) Vascular superoxide anion production was analysed by dihydroethidium staining of aortic cryosections. ( C ) Measurement of hydrogen peroxide formation in aortic tissue was performed using an amplex red-based HPLC assay ( n = 4–7). Statistical significance was calculated by one-way ANOVA and Tukey multiple comparison test ( A and C ). ( D ) Aortic rings from myelomonocytic cell-specific α1AMPK knockout mice (α1AMPK fl/fl x LysM-Cre + ) and corresponding wild-type littermates (LysM Cre/wt ) treated with ATII (1.0 mg/kg for 7 days) were incubated with PEG-SOD ex vivo ; endothelial-dependent relaxation in response to acetylcholine (ACh) was analysed by isometric tension studies ( n = 8 animals/group). ( E ) Phorbol ester (PDBu) stimulated oxidative burst in whole blood was determined by L-012 enhanced chemiluminescence ( n = 12). Statistical significance was calculated by two-way ANOVA and Tukey post hoc test (for detailed P , Figures S8 and S9 ). ( F ) Nox2 mRNA ( n = 4–6) and protein expression in aortic tissue. Pooled samples ( n = 3) of n = 6 mice. One-way ANOVA and Tukey multiple comparison test were used to calculate statistical significance. * P

Figure Legend Snippet: Vascular oxidative stress is increased in mice lacking myelomonocytic cell α1AMPK. ( A ) Aortic 3-nitrotyrosine staining was used as a surrogate for peroxynitrite formation and assessed by dot blot technique. Pooled samples ( n = 3) of n = 6 mice. ( B ) Vascular superoxide anion production was analysed by dihydroethidium staining of aortic cryosections. ( C ) Measurement of hydrogen peroxide formation in aortic tissue was performed using an amplex red-based HPLC assay ( n = 4–7). Statistical significance was calculated by one-way ANOVA and Tukey multiple comparison test ( A and C ). ( D ) Aortic rings from myelomonocytic cell-specific α1AMPK knockout mice (α1AMPK fl/fl x LysM-Cre + ) and corresponding wild-type littermates (LysM Cre/wt ) treated with ATII (1.0 mg/kg for 7 days) were incubated with PEG-SOD ex vivo ; endothelial-dependent relaxation in response to acetylcholine (ACh) was analysed by isometric tension studies ( n = 8 animals/group). ( E ) Phorbol ester (PDBu) stimulated oxidative burst in whole blood was determined by L-012 enhanced chemiluminescence ( n = 12). Statistical significance was calculated by two-way ANOVA and Tukey post hoc test (for detailed P , Figures S8 and S9 ). ( F ) Nox2 mRNA ( n = 4–6) and protein expression in aortic tissue. Pooled samples ( n = 3) of n = 6 mice. One-way ANOVA and Tukey multiple comparison test were used to calculate statistical significance. * P

Techniques Used: Mouse Assay, Staining, Dot Blot, High Performance Liquid Chromatography, Knock-Out, Incubation, Ex Vivo, Expressing

4) Product Images from "BCR-ABL tyrosine kinase inhibitors promote pathological changes in dilator phenotype in the human microvasculature"

Article Title: BCR-ABL tyrosine kinase inhibitors promote pathological changes in dilator phenotype in the human microvasculature

Journal: Microcirculation (New York, N.Y. : 1994)

doi: 10.1111/micc.12625

Flow-mediated dilation in the presence or absence of either L-NAME or PEG-Catalase. Panel A. Consistent with our previous work, in arterioles incubated in PBS vehicle, the nitric oxide synthase inhibitor L-NAME (n = 5) reduced FMD compared to control (n = 8) while the hydrogen peroxide scavenger PEG-Catalase had no effect on FMD (n = 7). In arterioles incubated with either imatinib (Panel B) or nilotinib (Panel C), the nitric oxide synthase inhibitor L-NAME (n = 7.4) had no effect on FMD compared to control (n = 7.7) while the hydrogen peroxide scavenger PEG-Catalase reduced FMD (n = 7.5). Area under the curve analysis is shown in Panel D. In imatinib- and nilotinib-treated vessels, the area under the curve for PEG-Catalase–inhibitable dilation was reduced compared to control. All data shown as mean ± SD. * P

Figure Legend Snippet: Flow-mediated dilation in the presence or absence of either L-NAME or PEG-Catalase. Panel A. Consistent with our previous work, in arterioles incubated in PBS vehicle, the nitric oxide synthase inhibitor L-NAME (n = 5) reduced FMD compared to control (n = 8) while the hydrogen peroxide scavenger PEG-Catalase had no effect on FMD (n = 7). In arterioles incubated with either imatinib (Panel B) or nilotinib (Panel C), the nitric oxide synthase inhibitor L-NAME (n = 7.4) had no effect on FMD compared to control (n = 7.7) while the hydrogen peroxide scavenger PEG-Catalase reduced FMD (n = 7.5). Area under the curve analysis is shown in Panel D. In imatinib- and nilotinib-treated vessels, the area under the curve for PEG-Catalase–inhibitable dilation was reduced compared to control. All data shown as mean ± SD. * P

Techniques Used: Incubation

5) Product Images from "ÃÂ±1AMPK deletion in myelomonocytic cells induces a pro-inflammatory phenotype and enhances angiotensin II-induced vascular dysfunction"

Article Title: ÃÂ±1AMPK deletion in myelomonocytic cells induces a pro-inflammatory phenotype and enhances angiotensin II-induced vascular dysfunction

Journal: Cardiovascular Research

doi: 10.1093/cvr/cvy172

Vascular oxidative stress is increased in mice lacking myelomonocytic cell ÃÂ±1AMPK. ( A ) Aortic 3-nitrotyrosine staining was used as a surrogate for peroxynitrite formation and assessed by dot blot technique. Pooled samples ( n = 3) of n = 6 mice. ( B ) Vascular superoxide anion production was analysed by dihydroethidium staining of aortic cryosections. ( C ) Measurement of hydrogen peroxide formation in aortic tissue was performed using an amplex red-based HPLC assay ( n = 4Ã¢ÂÂ7). Statistical significance was calculated by one-way ANOVA and Tukey multiple comparison test ( A and C ). ( D ) Aortic rings from myelomonocytic cell-specific ÃÂ±1AMPK knockout mice (ÃÂ±1AMPK fl/fl x LysM-Cre + ) and corresponding wild-type littermates (LysM Cre/wt ) treated with ATII (1.0 mg/kg for 7 days) were incubated with PEG-SOD ex vivo ; endothelial-dependent relaxation in response to acetylcholine (ACh) was analysed by isometric tension studies ( n = 8 animals/group). ( E ) Phorbol ester (PDBu) stimulated oxidative burst in whole blood was determined by L-012 enhanced chemiluminescence ( n = 12). Statistical significance was calculated by two-way ANOVA and Tukey post hoc test (for detailed P , Figures S8 and S9 ). ( F ) Nox2 mRNA ( n = 4Ã¢ÂÂ6) and protein expression in aortic tissue. Pooled samples ( n = 3) of n = 6 mice. One-way ANOVA and Tukey multiple comparison test were used to calculate statistical significance. * P

Figure Legend Snippet: Vascular oxidative stress is increased in mice lacking myelomonocytic cell ÃÂ±1AMPK. ( A ) Aortic 3-nitrotyrosine staining was used as a surrogate for peroxynitrite formation and assessed by dot blot technique. Pooled samples ( n = 3) of n = 6 mice. ( B ) Vascular superoxide anion production was analysed by dihydroethidium staining of aortic cryosections. ( C ) Measurement of hydrogen peroxide formation in aortic tissue was performed using an amplex red-based HPLC assay ( n = 4Ã¢ÂÂ7). Statistical significance was calculated by one-way ANOVA and Tukey multiple comparison test ( A and C ). ( D ) Aortic rings from myelomonocytic cell-specific ÃÂ±1AMPK knockout mice (ÃÂ±1AMPK fl/fl x LysM-Cre + ) and corresponding wild-type littermates (LysM Cre/wt ) treated with ATII (1.0 mg/kg for 7 days) were incubated with PEG-SOD ex vivo ; endothelial-dependent relaxation in response to acetylcholine (ACh) was analysed by isometric tension studies ( n = 8 animals/group). ( E ) Phorbol ester (PDBu) stimulated oxidative burst in whole blood was determined by L-012 enhanced chemiluminescence ( n = 12). Statistical significance was calculated by two-way ANOVA and Tukey post hoc test (for detailed P , Figures S8 and S9 ). ( F ) Nox2 mRNA ( n = 4Ã¢ÂÂ6) and protein expression in aortic tissue. Pooled samples ( n = 3) of n = 6 mice. One-way ANOVA and Tukey multiple comparison test were used to calculate statistical significance. * P

Techniques Used: Mouse Assay, Staining, Dot Blot, High Performance Liquid Chromatography, Knock-Out, Incubation, Ex Vivo, Expressing

6) Product Images from "Role of Mitochondrial Electron Transport Chain Complexes in Capsaicin Mediated Oxidative Stress Leading to Apoptosis in Pancreatic Cancer Cells"

Article Title: Role of Mitochondrial Electron Transport Chain Complexes in Capsaicin Mediated Oxidative Stress Leading to Apoptosis in Pancreatic Cancer Cells

Journal: PLoS ONE

doi: 10.1371/journal.pone.0020151

Anti-oxidants prevent capsaicin-induced apoptosis. ( A ) BxPC-3 cells were pretreated with PEG-SOD (100 U/ml), PEG-catalase (500 U/ml) or EUK-134 (50 µM) for 1 h and then treated with DMSO or 150 µM capsaicin for 24 h, ( B ) BxPC-3 ρ 0 cells were treated with DMSO or 150 µM capsaicin for 24 h, and apoptosis was determined using annexin-V/FITC and propidium iodide and analyzed by flow cytometery. Results are expressed as mean ± SD (n = 3) of three independent experiments. *Statistically different when compared with control ( P

Figure Legend Snippet: Anti-oxidants prevent capsaicin-induced apoptosis. ( A ) BxPC-3 cells were pretreated with PEG-SOD (100 U/ml), PEG-catalase (500 U/ml) or EUK-134 (50 µM) for 1 h and then treated with DMSO or 150 µM capsaicin for 24 h, ( B ) BxPC-3 ρ 0 cells were treated with DMSO or 150 µM capsaicin for 24 h, and apoptosis was determined using annexin-V/FITC and propidium iodide and analyzed by flow cytometery. Results are expressed as mean ± SD (n = 3) of three independent experiments. *Statistically different when compared with control ( P

Techniques Used: Flow Cytometry

7) Product Images from "The NADPH Oxidase Subunit p22phox Inhibits the Function of the Tumor Suppressor Protein Tuberin"

Article Title: The NADPH Oxidase Subunit p22phox Inhibits the Function of the Tumor Suppressor Protein Tuberin

Journal: The American Journal of Pathology

doi: 10.2353/ajpath.2010.090606

Superoxide is the major ROS involved in maintaining HIF-2α in the absence of VHL. A: Where indicated, antioxidants targeting hydrogen peroxide, PEG-Catalase (500 U/ml), NAC (100 mmol/L), or vehicle alone (−) were added to RCC 786-O cells

Figure Legend Snippet: Superoxide is the major ROS involved in maintaining HIF-2α in the absence of VHL. A: Where indicated, antioxidants targeting hydrogen peroxide, PEG-Catalase (500 U/ml), NAC (100 mmol/L), or vehicle alone (−) were added to RCC 786-O cells

Techniques Used:

8) Product Images from "TLR4 signaling induces TLR2 expression in endothelial cells via neutrophil NADPH oxidase"

Article Title: TLR4 signaling induces TLR2 expression in endothelial cells via neutrophil NADPH oxidase

Journal: Journal of Clinical Investigation

doi: 10.1172/JCI200318696

Augmented LPS induction of TLR2 in endothelial cells requires PMN NADPH oxidase and PMN adhesion. Studies determined the effects of PMNs cocultured with MLVECs on MLVEC TLR2 expression in response to LPS. MLVECs were isolated and cultured as described in Methods and treated with LPS (1 μg/ml) for 2 hours. The cocultured PMNs were isolated from WT and gp91 phox–/– mice, respectively, and were added at a concentration of 1 × 10 5 cells/ml. At the end of incubation with LPS, MLVECs were washed with HBSS three times and then lysed with lysis buffer. Cell lysates were subjected to extraction of total RNA and RT-PCR analysis ( a ) as well as Western blotting with anti-TLR2 antibody ( b ). To address the effects of CD18 on PMN-activated TLR2 expression in MLVECs, confluent MLVECs were treated with LPS in the presence of WT PMNs and anti-CD18 antibody for 2 hours, followed by washing with HBSS three times. This was followed by RT-PCR and Western analysis ( a and b , lane 6). ( c ) To address the role of endogenous endothelial NADPH oxidase in the regulation of TLR2 expression, MLVECs isolated from p47 phox–/– mice were stimulated with LPS and cocultured with or without WT PMNs for the times indicated. To address the role of oxidants derived from PMNs in LPS-induced TLR2 expression in endothelial cells, membrane-permeable PEG-catalase (1,000 U/ml) was applied to the coculture system. The data are representative of three independent studies.

Figure Legend Snippet: Augmented LPS induction of TLR2 in endothelial cells requires PMN NADPH oxidase and PMN adhesion. Studies determined the effects of PMNs cocultured with MLVECs on MLVEC TLR2 expression in response to LPS. MLVECs were isolated and cultured as described in Methods and treated with LPS (1 μg/ml) for 2 hours. The cocultured PMNs were isolated from WT and gp91 phox–/– mice, respectively, and were added at a concentration of 1 × 10 5 cells/ml. At the end of incubation with LPS, MLVECs were washed with HBSS three times and then lysed with lysis buffer. Cell lysates were subjected to extraction of total RNA and RT-PCR analysis ( a ) as well as Western blotting with anti-TLR2 antibody ( b ). To address the effects of CD18 on PMN-activated TLR2 expression in MLVECs, confluent MLVECs were treated with LPS in the presence of WT PMNs and anti-CD18 antibody for 2 hours, followed by washing with HBSS three times. This was followed by RT-PCR and Western analysis ( a and b , lane 6). ( c ) To address the role of endogenous endothelial NADPH oxidase in the regulation of TLR2 expression, MLVECs isolated from p47 phox–/– mice were stimulated with LPS and cocultured with or without WT PMNs for the times indicated. To address the role of oxidants derived from PMNs in LPS-induced TLR2 expression in endothelial cells, membrane-permeable PEG-catalase (1,000 U/ml) was applied to the coculture system. The data are representative of three independent studies.

Techniques Used: Expressing, Isolation, Cell Culture, Mouse Assay, Concentration Assay, Incubation, Lysis, Reverse Transcription Polymerase Chain Reaction, Western Blot, Derivative Assay

9) Product Images from "2-Deoxy-d-Glucose Combined with Cisplatin Enhances Cytotoxicity via Metabolic Oxidative Stress in Human Head and Neck Cancer Cells"

Article Title: 2-Deoxy-d-Glucose Combined with Cisplatin Enhances Cytotoxicity via Metabolic Oxidative Stress in Human Head and Neck Cancer Cells

Journal: Cancer research

doi: 10.1158/0008-5472.CAN-06-3717

Effect of PEG-SOD and PEG-catalase on 2DG toxicity in FaDu cells. Cells were treated with 18 ÃÂ¼mol/L PEG, 100 units/mL PEG-SOD, 100 units/mL PEG-catalase ( PEG-CAT ), or 50 units/mL PEG-SOD + 50 units/mL PEG-catalase for 1 h before and during treatment

Figure Legend Snippet: Effect of PEG-SOD and PEG-catalase on 2DG toxicity in FaDu cells. Cells were treated with 18 ÃÂ¼mol/L PEG, 100 units/mL PEG-SOD, 100 units/mL PEG-catalase ( PEG-CAT ), or 50 units/mL PEG-SOD + 50 units/mL PEG-catalase for 1 h before and during treatment

Techniques Used:

10) Product Images from "Release of cellular tension signals self-restorative ventral lamellipodia to heal barrier micro-wounds"

Article Title: Release of cellular tension signals self-restorative ventral lamellipodia to heal barrier micro-wounds

Journal: The Journal of Cell Biology

doi: 10.1083/jcb.201209077

VL are enriched in and functionally dependent on NADPH oxidase activity. (a) MVECs coexpressing p47phox-DsRed and actin-GFP were imaged live during T cell diapedesis. p47phox was enriched in ventral (IRM) actin-rich initiation nodes (N) and in VL leading edge (arrowheads). See Video 10 . (b) Representative ratiometric images of H 2 O 2 production in (i) pore- and (ii) gap-closing VL in MVECs expressing the biosensor mHyPer during T cell diapedesis. (c) Quantification of p47phox (i) and H 2 O 2 (ii) enrichment in VL. n > 13. (d, i) Representative NADPH oxidase inhibition/washout imaging experiment. After multiple T cell diapedesis events on MVECs expressing mYFP, apocynin was added. Arrows indicate multiple pores and gaps that persisted for 15 min, but were rapidly healed by steered VL (arrowheads) after drug washout. See Video 10. Experiments as in d (i) were performed with VAS-2870, DPI, PEG-catalase, and DMSO (control) and quantified by cumulative wound closure analysis, shown as a continuous line plot (ii) and bar graph of single pre/post-washout time points (iii). n > 5. (e) MVECs coexpressing mDsRed and mHyPer were imaged during probe wounds and after addition of VAS-2870. Representative mDsRed images (i), kymograph (ii), mHyper ratiometic images (iii), and quantitation (iv) are shown. n = 3. Values represent mean ± SEM. Statistical significance is indicated with p-values as follows: ***, P

Figure Legend Snippet: VL are enriched in and functionally dependent on NADPH oxidase activity. (a) MVECs coexpressing p47phox-DsRed and actin-GFP were imaged live during T cell diapedesis. p47phox was enriched in ventral (IRM) actin-rich initiation nodes (N) and in VL leading edge (arrowheads). See Video 10 . (b) Representative ratiometric images of H 2 O 2 production in (i) pore- and (ii) gap-closing VL in MVECs expressing the biosensor mHyPer during T cell diapedesis. (c) Quantification of p47phox (i) and H 2 O 2 (ii) enrichment in VL. n > 13. (d, i) Representative NADPH oxidase inhibition/washout imaging experiment. After multiple T cell diapedesis events on MVECs expressing mYFP, apocynin was added. Arrows indicate multiple pores and gaps that persisted for 15 min, but were rapidly healed by steered VL (arrowheads) after drug washout. See Video 10. Experiments as in d (i) were performed with VAS-2870, DPI, PEG-catalase, and DMSO (control) and quantified by cumulative wound closure analysis, shown as a continuous line plot (ii) and bar graph of single pre/post-washout time points (iii). n > 5. (e) MVECs coexpressing mDsRed and mHyPer were imaged during probe wounds and after addition of VAS-2870. Representative mDsRed images (i), kymograph (ii), mHyper ratiometic images (iii), and quantitation (iv) are shown. n = 3. Values represent mean ± SEM. Statistical significance is indicated with p-values as follows: ***, P

Techniques Used: Activity Assay, Expressing, Inhibition, Imaging, Quantitation Assay

11) Product Images from "Increased mitochondrial ROS generation mediates the loss of the anti‐contractile effects of perivascular adipose tissue in high‐fat diet obese mice) Increased mitochondrial ROS generation mediates the loss of the anti‐contractile effects of perivascular adipose tissue in high‐fat diet obese mice"

Article Title: Increased mitochondrial ROS generation mediates the loss of the anti‐contractile effects of perivascular adipose tissue in high‐fat diet obese mice) Increased mitochondrial ROS generation mediates the loss of the anti‐contractile effects of perivascular adipose tissue in high‐fat diet obese mice

Journal: British Journal of Pharmacology

doi: 10.1111/bph.13687

Mitochondria are a potential source of increased ROS in PVAT from obese mice, and mitochondria‐derived ROS alter the expression of antioxidant enzymes in PVAT. Concentration–effect curves to PE were performed in endothelium‐denuded aortic rings from control [( A and C ) n = 8 for each experimental group] and obese [( B and D ) n = 8 for each experimental group] mice. The role of mROS on PVAT modulation of aortic smooth muscle contraction was investigated using MnTMPyP (3 × 10 −5 M), a mitochondria‐targeted superoxide scavenger and PEG‐catalase (Peg‐cat; 200 U·mL −1 ), which dismutates mitochondria‐derived H 2 O 2 . Protein expression and activity of the antioxidant enzymes SOD‐Mn [( E and G ) n = 5 in both groups] and catalase [( F and H ) n = 5 in both groups] were determined by Western blot and SOD‐Mn and catalase activity assay kits, respectively, in PVAT from control and obese mice. Representative Western blots are shown in the upper panels, with quantitative analysis in the lower panels. Results were normalized to β‐actin expression and are expressed as relative units. Results represent the mean ± SEM. * P

Figure Legend Snippet: Mitochondria are a potential source of increased ROS in PVAT from obese mice, and mitochondria‐derived ROS alter the expression of antioxidant enzymes in PVAT. Concentration–effect curves to PE were performed in endothelium‐denuded aortic rings from control [( A and C ) n = 8 for each experimental group] and obese [( B and D ) n = 8 for each experimental group] mice. The role of mROS on PVAT modulation of aortic smooth muscle contraction was investigated using MnTMPyP (3 × 10 −5 M), a mitochondria‐targeted superoxide scavenger and PEG‐catalase (Peg‐cat; 200 U·mL −1 ), which dismutates mitochondria‐derived H 2 O 2 . Protein expression and activity of the antioxidant enzymes SOD‐Mn [( E and G ) n = 5 in both groups] and catalase [( F and H ) n = 5 in both groups] were determined by Western blot and SOD‐Mn and catalase activity assay kits, respectively, in PVAT from control and obese mice. Representative Western blots are shown in the upper panels, with quantitative analysis in the lower panels. Results were normalized to β‐actin expression and are expressed as relative units. Results represent the mean ± SEM. * P

Techniques Used: Mouse Assay, Derivative Assay, Expressing, Concentration Assay, Activity Assay, Western Blot

12) Product Images from "Chronic hypoxia limits H2O2-induced inhibition of ASIC1-dependent store-operated calcium entry in pulmonary arterial smooth muscle"

Article Title: Chronic hypoxia limits H2O2-induced inhibition of ASIC1-dependent store-operated calcium entry in pulmonary arterial smooth muscle

Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

doi: 10.1152/ajplung.00095.2014

CH increases pulmonary arterial antioxidant capacity. A : Amplex Red RFU from control intrapulmonary arteries following treatment with PEG-SOD (50 U/ml), the SOD mimetic, tiron (10 mM), or inhibition of catalase and glutathione peroxidase (GPx) with 3-amino-1,2,4-triazole (AT; 5 mM) and mercaptosuccinic acid (MSA; 3 mM) are within the linear range of the background-subtracted standard curve. B : summary data of H 2 O 2 levels in intrapulmonary arteries from control and CH rats following above treatments. C : rate of H 2 O 2 catalysis (1 μM) by control and CH intrapulmonary arteries measured by Amplex Red fluorescence. Values are means ± SE; n = 6–8 animals per group; τ P

Figure Legend Snippet: CH increases pulmonary arterial antioxidant capacity. A : Amplex Red RFU from control intrapulmonary arteries following treatment with PEG-SOD (50 U/ml), the SOD mimetic, tiron (10 mM), or inhibition of catalase and glutathione peroxidase (GPx) with 3-amino-1,2,4-triazole (AT; 5 mM) and mercaptosuccinic acid (MSA; 3 mM) are within the linear range of the background-subtracted standard curve. B : summary data of H 2 O 2 levels in intrapulmonary arteries from control and CH rats following above treatments. C : rate of H 2 O 2 catalysis (1 μM) by control and CH intrapulmonary arteries measured by Amplex Red fluorescence. Values are means ± SE; n = 6–8 animals per group; τ P

Techniques Used: Inhibition, Fluorescence

Di-(4-carboxybenzyl) hyponitrite (SOTS-1) increases PASMC O 2 ·− levels. Representative images ( A ) and summary data ( B ) showing background-subtracted MFI of DHE in PASMC from control rats treated with increasing concentrations of SOTS-1 (0.01, 0.1, 1.0 mM) or SOTS-1 (0.01 mM) plus PEG-SOD (50 U/ml) or PEG-catalase (250 U/ml). Fluorescence images were digitally inverted to provide better contrast and visibility of immunofluorescence. Values are means ± SE; n = 3–5 animals per group. ** P

Figure Legend Snippet: Di-(4-carboxybenzyl) hyponitrite (SOTS-1) increases PASMC O 2 ·− levels. Representative images ( A ) and summary data ( B ) showing background-subtracted MFI of DHE in PASMC from control rats treated with increasing concentrations of SOTS-1 (0.01, 0.1, 1.0 mM) or SOTS-1 (0.01 mM) plus PEG-SOD (50 U/ml) or PEG-catalase (250 U/ml). Fluorescence images were digitally inverted to provide better contrast and visibility of immunofluorescence. Values are means ± SE; n = 3–5 animals per group. ** P

Techniques Used: Fluorescence, Immunofluorescence

13) Product Images from "Role of ER Stress Response in Photodynamic Therapy: ROS Generated in Different Subcellular Compartments Trigger Diverse Cell Death Pathways"

Article Title: Role of ER Stress Response in Photodynamic Therapy: ROS Generated in Different Subcellular Compartments Trigger Diverse Cell Death Pathways

Journal: PLoS ONE

doi: 10.1371/journal.pone.0032972

Role of ROS generation in EG-porphyrin-mediated cell death. ( A ) Effect ROS scavengers on cell viability after PDT. 4T1 cells were loaded with EG-porphyrin derivatives for 16 h, washed and then pre-incubated for 1 h with L-histidine (20 mM), trolox (5 mM), NAC (15 mM), tiron (10 mM), DMSO (1%), PEG-catalase (300 U/ml) and sodium pyruvate (Na Pyruv) (10 mM) before light exposure. Similarly, HL60 cells were pre-incubated with L-histidine (20 mM), trolox (4 mM), NAC (5 mM), tiron (10 mM), DMSO (1%), PEG-catalase (300 U/ml) and sodium pyruvate (Na Pyruv) (10 mM). After irradiation the cells were further cultivated and cell viability was determined 24 h post-PDT by the trypan blue exclusion method. Cells treated with EG-porphyrin derivatives without irradiation were used as controls (dark). The percentage of dead cells was expressed as the mean ± SD (n = 3). *P

Figure Legend Snippet: Role of ROS generation in EG-porphyrin-mediated cell death. ( A ) Effect ROS scavengers on cell viability after PDT. 4T1 cells were loaded with EG-porphyrin derivatives for 16 h, washed and then pre-incubated for 1 h with L-histidine (20 mM), trolox (5 mM), NAC (15 mM), tiron (10 mM), DMSO (1%), PEG-catalase (300 U/ml) and sodium pyruvate (Na Pyruv) (10 mM) before light exposure. Similarly, HL60 cells were pre-incubated with L-histidine (20 mM), trolox (4 mM), NAC (5 mM), tiron (10 mM), DMSO (1%), PEG-catalase (300 U/ml) and sodium pyruvate (Na Pyruv) (10 mM). After irradiation the cells were further cultivated and cell viability was determined 24 h post-PDT by the trypan blue exclusion method. Cells treated with EG-porphyrin derivatives without irradiation were used as controls (dark). The percentage of dead cells was expressed as the mean ± SD (n = 3). *P

Techniques Used: Incubation, Irradiation

14) Product Images from "Pressor Effect of Apelin-13 in the Rostral Ventrolateral Medulla: Role of NAD(P)H Oxidase-Derived Superoxide"

Article Title: Pressor Effect of Apelin-13 in the Rostral Ventrolateral Medulla: Role of NAD(P)H Oxidase-Derived Superoxide

Journal: The Journal of Pharmacology and Experimental Therapeutics

doi: 10.1124/jpet.110.174102

Identification of ROS involved in the chronotropic actions of apelin-13 in neurons. A, role of superoxide. The neuronal firing rate was recorded in neurons treated under the following conditions: superfusion of PBS control (Con); superfusion of apelin-13 (APLN, 100 nM) followed by washout of apelin-13 with fresh superfusate solution; superfusion of PEG-SOD (SOD, 25 U/ml), and PEG-SOD plus apelin-13 (SOD+APLN). Data are mean ± S.E. ( n = 9 neurons). B, effect of xanthine-xanthine oxidase on neuronal firing rate. The neuronal firing rate was recorded in neurons treated under PBS control (Con) and superfusion of xanthine-xanthine oxidase (10 mM and 20 mU/ml). Data are mean ± S.E. ( n = 5 neurons). C, role of hydrogen peroxide. The neuronal firing rate was recorded in neurons treated under the following conditions: superfusion of PBS control (Con); superfusion of apelin-13 (APLN, 100 nM) followed by washout of apelin-13 with fresh superfusate solution, superfusion of PEG-catalase (CAT, 250 U/ml), and PEG-catalase plus apelin-13 (CAT+APLN). Data are mean ± S.E. ( n = 7 neurons). D, effect of hydrogen peroxide on neuronal firing rate. Data are mean ± S.E. of neuronal firing rate in eight neurons treated under PBS control (Con) and superfusion of hydrogen peroxide (H 2 O 2 , 1 μM). *, P

Figure Legend Snippet: Identification of ROS involved in the chronotropic actions of apelin-13 in neurons. A, role of superoxide. The neuronal firing rate was recorded in neurons treated under the following conditions: superfusion of PBS control (Con); superfusion of apelin-13 (APLN, 100 nM) followed by washout of apelin-13 with fresh superfusate solution; superfusion of PEG-SOD (SOD, 25 U/ml), and PEG-SOD plus apelin-13 (SOD+APLN). Data are mean ± S.E. ( n = 9 neurons). B, effect of xanthine-xanthine oxidase on neuronal firing rate. The neuronal firing rate was recorded in neurons treated under PBS control (Con) and superfusion of xanthine-xanthine oxidase (10 mM and 20 mU/ml). Data are mean ± S.E. ( n = 5 neurons). C, role of hydrogen peroxide. The neuronal firing rate was recorded in neurons treated under the following conditions: superfusion of PBS control (Con); superfusion of apelin-13 (APLN, 100 nM) followed by washout of apelin-13 with fresh superfusate solution, superfusion of PEG-catalase (CAT, 250 U/ml), and PEG-catalase plus apelin-13 (CAT+APLN). Data are mean ± S.E. ( n = 7 neurons). D, effect of hydrogen peroxide on neuronal firing rate. Data are mean ± S.E. of neuronal firing rate in eight neurons treated under PBS control (Con) and superfusion of hydrogen peroxide (H 2 O 2 , 1 μM). *, P

Techniques Used:

15) Product Images from "Platelet hyperaggregability in high-fat fed rats: A role for intraplatelet reactive-oxygen species production"

Article Title: Platelet hyperaggregability in high-fat fed rats: A role for intraplatelet reactive-oxygen species production

Journal: Cardiovascular Diabetology

doi: 10.1186/1475-2840-11-5

Effect of high-fat diet in the generation of intraplatelet reactive-oxygen species (ROS) . Male Wistar rats were fed with either a standard chow diet (SCD) or high-fat diet (HFD) during 10 weeks. Washed platelets (1.2 × 10 8 platelets/ml) from SCD or HFF rats were pre-incubated with N-acetylcysteine (NAC, 1 mM for 15 min) or PEG-catalase (1000 mU/ml, 15 min) and then stimulated with ADP (10 μM). Generation of ROS was quantified by flow cytometry using 2'-7'-dichloroflurescin diacetate (DCFH-DA). Results are shown as mean ± SEM values for n = 6-7. * P

Figure Legend Snippet: Effect of high-fat diet in the generation of intraplatelet reactive-oxygen species (ROS) . Male Wistar rats were fed with either a standard chow diet (SCD) or high-fat diet (HFD) during 10 weeks. Washed platelets (1.2 × 10 8 platelets/ml) from SCD or HFF rats were pre-incubated with N-acetylcysteine (NAC, 1 mM for 15 min) or PEG-catalase (1000 mU/ml, 15 min) and then stimulated with ADP (10 μM). Generation of ROS was quantified by flow cytometry using 2'-7'-dichloroflurescin diacetate (DCFH-DA). Results are shown as mean ± SEM values for n = 6-7. * P

Techniques Used: Incubation, Flow Cytometry, Cytometry

Effect of N-Acetylcysteine (NAC) and PEG-catalase on washed platelet aggregation of rats fed with a standard chow diet (SCD) or high-fat diet (HFD) during 10 weeks . Washed platelets (1.2 × 10 8 platelets/ml) from SCD or HFD rats were stimulated with thrombin (100 mU/ml; panel A) or ADP (10 μM; panel B) in the absence or the presence of NAC (1 mM) or PEG-catalase (1000 U/ml). Results are shown as mean ± SEM values ( n = 4-7). * P

Figure Legend Snippet: Effect of N-Acetylcysteine (NAC) and PEG-catalase on washed platelet aggregation of rats fed with a standard chow diet (SCD) or high-fat diet (HFD) during 10 weeks . Washed platelets (1.2 × 10 8 platelets/ml) from SCD or HFD rats were stimulated with thrombin (100 mU/ml; panel A) or ADP (10 μM; panel B) in the absence or the presence of NAC (1 mM) or PEG-catalase (1000 U/ml). Results are shown as mean ± SEM values ( n = 4-7). * P

Techniques Used:

16) Product Images from "Reactive Oxygen Species Are Involved in Regulating Hypocontractility of Mesenteric Artery to Norepinephrine in Cirrhotic Rats with Portal Hypertension"

Article Title: Reactive Oxygen Species Are Involved in Regulating Hypocontractility of Mesenteric Artery to Norepinephrine in Cirrhotic Rats with Portal Hypertension

Journal: International Journal of Biological Sciences

doi: 10.7150/ijbs.8081

Dose-response curves of isolated mesenteric artery contractility to norepinephrine with different concentrations. Vasoconstriction rate and the logarithm of norepinephrine concentration were used as vertical axis and abscissa, respectively. The results showed that dose-response curve of mesenteric arteriole contractility to norepinephrine moved to the left and EC 50 decreased in rats with cirrhosis in apocynin ( A, B ) or PEG-catalase ( C, D ) treatment. A: * PHTA compared with PHTC, P

Figure Legend Snippet: Dose-response curves of isolated mesenteric artery contractility to norepinephrine with different concentrations. Vasoconstriction rate and the logarithm of norepinephrine concentration were used as vertical axis and abscissa, respectively. The results showed that dose-response curve of mesenteric arteriole contractility to norepinephrine moved to the left and EC 50 decreased in rats with cirrhosis in apocynin ( A, B ) or PEG-catalase ( C, D ) treatment. A: * PHTA compared with PHTC, P

Techniques Used: Isolation, Concentration Assay

Fluorescence intensity of vascular wall in rats after drugs treatment. ( A ) Fluorescence intensity was the strongest in cirrhotic rats and diminished by treatment with apocynin, tempol or PEG-catalase. Each image is representative of results from 6 different animals. ( B ) The quantitative of fluorescence intensity was analyzed in rats after treatment with different drugs. Values are mean ± SEM; n=6 for each group. **: compared with NC, P

Figure Legend Snippet: Fluorescence intensity of vascular wall in rats after drugs treatment. ( A ) Fluorescence intensity was the strongest in cirrhotic rats and diminished by treatment with apocynin, tempol or PEG-catalase. Each image is representative of results from 6 different animals. ( B ) The quantitative of fluorescence intensity was analyzed in rats after treatment with different drugs. Values are mean ± SEM; n=6 for each group. **: compared with NC, P

Techniques Used: Fluorescence

17) Product Images from "Enhanced Renal Afferent Arteriolar Reactive Oxygen Species and Contractility to Endothelin-1 Are Associated with Canonical Wnt Signaling in Diabetic Mice"

Article Title: Enhanced Renal Afferent Arteriolar Reactive Oxygen Species and Contractility to Endothelin-1 Are Associated with Canonical Wnt Signaling in Diabetic Mice

Journal: Kidney & blood pressure research

doi: 10.1159/000490334

Techniques Used: Mouse Assay

18) Product Images from "Hydrogen Peroxide Regulates Extracellular Superoxide Dismutase Activity and Expression in Neonatal Pulmonary Hypertension"

Article Title: Hydrogen Peroxide Regulates Extracellular Superoxide Dismutase Activity and Expression in Neonatal Pulmonary Hypertension

Journal: Antioxidants & Redox Signaling

doi: 10.1089/ars.2010.3630

PEG-catalase decreases superoxide levels in resistance PAs. (A) Frozen lung sections from PPHN lambs ventilated for 24 h with 100% oxygen alone (L100; n = 7) or in combination with 20,000 U/kg PEG-catalase administered

Figure Legend Snippet: PEG-catalase decreases superoxide levels in resistance PAs. (A) Frozen lung sections from PPHN lambs ventilated for 24 h with 100% oxygen alone (L100; n = 7) or in combination with 20,000 U/kg PEG-catalase administered

Techniques Used:

PEG-catalase decreases ecSOD expression but increases activity in PPHN lungs. Lung tissue was harvested from fetal control and fetal PPHN lambs ( n = 6 each), and from PPHN lambs ventilated for 24 h with 100% O 2 alone (L100; n = 7)

Figure Legend Snippet: PEG-catalase decreases ecSOD expression but increases activity in PPHN lungs. Lung tissue was harvested from fetal control and fetal PPHN lambs ( n = 6 each), and from PPHN lambs ventilated for 24 h with 100% O 2 alone (L100; n = 7)

Techniques Used: Expressing, Activity Assay

PEG-catalase restores ecSOD activity in PPHN PASMCs. PASMCs isolated from PPHN lambs were treated with 0–200 U/ml PEG-catalase for 24 h in serum-free medium. ecSOD protein was purified from cell extracts with affinity chromatography,

Figure Legend Snippet: PEG-catalase restores ecSOD activity in PPHN PASMCs. PASMCs isolated from PPHN lambs were treated with 0–200 U/ml PEG-catalase for 24 h in serum-free medium. ecSOD protein was purified from cell extracts with affinity chromatography,

Techniques Used: Activity Assay, Isolation, Purification, Affinity Chromatography

PEG-catalase improves the arterial-to-alveolar oxygenation (a/A) ratio in PPHN lambs. The a/A ratio was calculated over a 24-h period for lambs with PPHN ventilated with 100% oxygen alone ( n = 12) or with 100% oxygen in combination with

Figure Legend Snippet: PEG-catalase improves the arterial-to-alveolar oxygenation (a/A) ratio in PPHN lambs. The a/A ratio was calculated over a 24-h period for lambs with PPHN ventilated with 100% oxygen alone ( n = 12) or with 100% oxygen in combination with

Techniques Used:

19) Product Images from "Juglanthraquinone C Induces Intracellular ROS Increase and Apoptosis by Activating the Akt/Foxo Signal Pathway in HCC Cells"

Article Title: Juglanthraquinone C Induces Intracellular ROS Increase and Apoptosis by Activating the Akt/Foxo Signal Pathway in HCC Cells

Journal: Oxidative Medicine and Cellular Longevity

doi: 10.1155/2016/4941623

JC induces apoptosis by increasing intracellular ROS. (a, c) Effect of JC on the total ROS levels in HepG2 and BEL-7402 cells was examined by flow cytometry. HepG2 cells were treated with DMSO or 8 μ g/mL JC for 12, 24, 36, and 48 hours (a). BEL-7402 cells were treated with DMSO or 6.7, 8.7, and 10.5 μ g/mL of JC for 12 hours (c). (b) Effect of JC on superoxide anion levels in HepG2 cells was examined by flow cytometry. The levels of ROS in HepG2 cells were treated with either DMSO or 8 μ g/mL of JC for 12, 24, 36, and 48 hours and analyzed by flow cytometry. (d–f) Effects of JC on catalase and SOD2 expression and Akt activation were determined by Western blot analysis. HepG2 cells were treated with either DMSO or 8 μ g/mL of JC for the indicated times (d and e). BEL-7402 cells were treated with DMSO or 8.7 μ g/mL of JC for the indicated times (f). GAPDH was used as a loading control. (g–j) NAC and PEG-catalase abrogate JC-induced apoptosis. HepG2 cells were pretreated with NAC and PEG-catalase for 1 hour. HepG2 cells were treated with either DMSO or 8 μ g/mL of JC for 36 hours and detected by Western blot analysis (g) or flow cytometry analysis (h). GAPDH was used as a loading control. BEL-7402 cells were treated with either DMSO or 8.7 μ g/mL of JC for 24 hours and detected by flow cytometry analysis (i and j).

Figure Legend Snippet: JC induces apoptosis by increasing intracellular ROS. (a, c) Effect of JC on the total ROS levels in HepG2 and BEL-7402 cells was examined by flow cytometry. HepG2 cells were treated with DMSO or 8 μ g/mL JC for 12, 24, 36, and 48 hours (a). BEL-7402 cells were treated with DMSO or 6.7, 8.7, and 10.5 μ g/mL of JC for 12 hours (c). (b) Effect of JC on superoxide anion levels in HepG2 cells was examined by flow cytometry. The levels of ROS in HepG2 cells were treated with either DMSO or 8 μ g/mL of JC for 12, 24, 36, and 48 hours and analyzed by flow cytometry. (d–f) Effects of JC on catalase and SOD2 expression and Akt activation were determined by Western blot analysis. HepG2 cells were treated with either DMSO or 8 μ g/mL of JC for the indicated times (d and e). BEL-7402 cells were treated with DMSO or 8.7 μ g/mL of JC for the indicated times (f). GAPDH was used as a loading control. (g–j) NAC and PEG-catalase abrogate JC-induced apoptosis. HepG2 cells were pretreated with NAC and PEG-catalase for 1 hour. HepG2 cells were treated with either DMSO or 8 μ g/mL of JC for 36 hours and detected by Western blot analysis (g) or flow cytometry analysis (h). GAPDH was used as a loading control. BEL-7402 cells were treated with either DMSO or 8.7 μ g/mL of JC for 24 hours and detected by flow cytometry analysis (i and j).

Techniques Used: Flow Cytometry, Cytometry, Expressing, Activation Assay, Western Blot

20) Product Images from "SIRT2 Interacts with β-catenin to Inhibit Wnt Signaling Output in Response to Radiation-Induced Stress"

Article Title: SIRT2 Interacts with β-catenin to Inhibit Wnt Signaling Output in Response to Radiation-Induced Stress

Journal: Molecular cancer research : MCR

doi: 10.1158/1541-7786.MCR-14-0223-T

$SIRT2 interacts directly with β-catenin. A, coimmunoprecipitation showing association of SIRT2 and β-catenin increases with IR. Sirt2 WT MEFs were exposed to single fractions of 2Gy, 5 Gy and 10 Gy, and compared to sham controls. Cells were harvested 24h after radiation and immunoprecipitated either with normal rabbit IgG control, SIRT2 or β-catenin antibodies. Bound proteins were analyzed by immunoblot with β-catenin antibody. B, coimmunoprecipitation analysis showing SIRT2 associates with β-catenin in PC-3 cells. C, coimmunoprecipitation analysis showing overexpressed Flag-SIRT2 binds to β-catenin. Protein lysates from U87 glioma cells stably expressing either pcDNA3 or Flag- SIRT2 were subjected to immunoprecipitation using rabbit IgG, DDK or β-catenin antibodies. Bound proteins were analyzed by immunoblot with β-catenin antibody. D, ROS measurement. Sirt2 WT and KO MEFs were labeled with H 2 DCFDA or carboxy DCFDA for 30 min before exposure to a single fraction of 10 Gy compared to sham controls. Cells were harvested after 30 min and analyzed. Treatment with PEG-catalase was used to scavenge ROS generated by radiation. E, Clonogenic survival assay. Sirt2 WT and KO cells were plated for clonogenic survival assay and treated with 200U/ml PEG-cat for 2h, followed by radiation. PEG-cat was left for the duration of the assay. Values represent the mean +/− SEM. *, P$
Figure Legend Snippet: SIRT2 interacts directly with β-catenin. A, coimmunoprecipitation showing association of SIRT2 and β-catenin increases with IR. Sirt2 WT MEFs were exposed to single fractions of 2Gy, 5 Gy and 10 Gy, and compared to sham controls. Cells were harvested 24h after radiation and immunoprecipitated either with normal rabbit IgG control, SIRT2 or β-catenin antibodies. Bound proteins were analyzed by immunoblot with β-catenin antibody. B, coimmunoprecipitation analysis showing SIRT2 associates with β-catenin in PC-3 cells. C, coimmunoprecipitation analysis showing overexpressed Flag-SIRT2 binds to β-catenin. Protein lysates from U87 glioma cells stably expressing either pcDNA3 or Flag- SIRT2 were subjected to immunoprecipitation using rabbit IgG, DDK or β-catenin antibodies. Bound proteins were analyzed by immunoblot with β-catenin antibody. D, ROS measurement. Sirt2 WT and KO MEFs were labeled with H 2 DCFDA or carboxy DCFDA for 30 min before exposure to a single fraction of 10 Gy compared to sham controls. Cells were harvested after 30 min and analyzed. Treatment with PEG-catalase was used to scavenge ROS generated by radiation. E, Clonogenic survival assay. Sirt2 WT and KO cells were plated for clonogenic survival assay and treated with 200U/ml PEG-cat for 2h, followed by radiation. PEG-cat was left for the duration of the assay. Values represent the mean +/− SEM. *, P

Techniques Used: Immunoprecipitation, Stable Transfection, Expressing, Labeling, Generated, Clonogenic Cell Survival Assay

21) Product Images from "Tumor Necrosis Factor–Related Apoptosis‐Inducing Ligand ( TRAIL) Promotes Angiogenesis and Ischemia‐Induced Neovascularization Via NADPH Oxidase 4 (NOX4) and Nitric Oxide–Dependent Mechanisms"

Article Title: Tumor Necrosis Factor–Related Apoptosis‐Inducing Ligand ( TRAIL) Promotes Angiogenesis and Ischemia‐Induced Neovascularization Via NADPH Oxidase 4 (NOX4) and Nitric Oxide–Dependent Mechanisms

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

doi: 10.1161/JAHA.115.002527

TRAIL and FGF ‐2‐inducible proliferation, migration, and tubule formation involves H 2 O 2 and NO . A, TRAIL ‐inducible proliferation and (B) migration involves H 2 O 2 and NO . Growth quiescent HMEC ‐1 cells were treated with PEG ‐Catalase ( PEG ‐Cat; 200 U/mL) and l ‐ NAME (1 mmol/L) for 1 hour prior to 10 ng/mL TRAIL treatment. Cell counts were assessed 72 hours later and migration assessed 24 hours later. C, TRAIL ‐inducible tubule formation involves H 2 O 2 and NO . Serum‐starved HMEC ‐1 cells were seeded in growth factor reduced Matrigel. Cells were treated with TRAIL (10 ng/mL) and PEG ‐Cat (200 U/mL) or l ‐ NAME (1 mmol/L). Tubule formation was photographed and quantified 3 hours later. FGF ‐2‐inducible (D) proliferation, (E) migration, and (F) tubule formation involves H 2 O 2 and NO . Treatment with FGF ‐2 was identical to above except that 50 ng/mL FGF ‐2 was used. Data represent the combined results of at least 3 independent experiments. Results are expressed as mean± SEM ; 1‐way ANOVA ; * P

Figure Legend Snippet: TRAIL and FGF ‐2‐inducible proliferation, migration, and tubule formation involves H 2 O 2 and NO . A, TRAIL ‐inducible proliferation and (B) migration involves H 2 O 2 and NO . Growth quiescent HMEC ‐1 cells were treated with PEG ‐Catalase ( PEG ‐Cat; 200 U/mL) and l ‐ NAME (1 mmol/L) for 1 hour prior to 10 ng/mL TRAIL treatment. Cell counts were assessed 72 hours later and migration assessed 24 hours later. C, TRAIL ‐inducible tubule formation involves H 2 O 2 and NO . Serum‐starved HMEC ‐1 cells were seeded in growth factor reduced Matrigel. Cells were treated with TRAIL (10 ng/mL) and PEG ‐Cat (200 U/mL) or l ‐ NAME (1 mmol/L). Tubule formation was photographed and quantified 3 hours later. FGF ‐2‐inducible (D) proliferation, (E) migration, and (F) tubule formation involves H 2 O 2 and NO . Treatment with FGF ‐2 was identical to above except that 50 ng/mL FGF ‐2 was used. Data represent the combined results of at least 3 independent experiments. Results are expressed as mean± SEM ; 1‐way ANOVA ; * P

Techniques Used: Migration

other:

Article Title: Oxidative Dimerization of PHD2 is Responsible for its Inactivation and Contributes to Metabolic Reprogramming via HIF-1α Activation
Article Snippet: Reagents and antibodies N -acetyl-l -cysteine (NAC), diamide, hydrogen peroxide (H2 O2 ), MG132, PEG-catalase, tert -butyl hydroperoxide (T-hydro) and 2′–7′–dichrolodihydrofluorescein diacetate (DCF-DA) were purchased from Sigma Aldrich and Invitrogen.

Incubation:

Article Title: Oleoyl-Lysophosphatidylcholine Limits Endothelial Nitric Oxide Bioavailability by Induction of Reactive Oxygen Species
Article Snippet: .. Cells were washed once with warm PBS, followed by incubation with 300 µL of pre-warmed assay buffer [HEPES-buffered Tyrode's solution (no FBS) containing 50 µM Amplex Red (Invitrogen) and 2 U/mL Horse Radish Peroxidase (Sigma)] containing 10 µM LPC 18:1 or PBS (vehicle) for 15 min. Polyethylene glycol catalase (PEG-catalase) 300 U/mL or polyethylene glycol superoxide dismutase (PEG-SOD) 75 U/mL (both Sigma) were added in order to detect catalase-sensitive peroxides and superoxide radicals in the medium. .. The buffer was then transferred to a black 96 well plate and fluorescence was measured at excitation and emission wavelengths of 540 and 580 nm, respectively.

BIA-KA:

Article Title: Enhanced Renal Afferent Arteriolar Reactive Oxygen Species and Contractility to Endothelin-1 Are Associated with Canonical Wnt Signaling in Diabetic Mice
Article Snippet: The probed bands were visualized by enhanced chemiluminescent substrates (ECL, Thermo Scientific) and analyzed by using Image J software (National Institutes of Health, Bethesda, MD). .. Chemicals and reagents Reagent sources were as follows: DMEM, sulindac, ET-1, PEG-catalase, PEG-SOD, apocynin (Sigma-Aldrich, St Louis, MO); DHE, C-H2 DCFDA (Invitrogen Life Technologies, Eugene, Dregon, USA); BCA protein assay kit, H2 O2 assay kit, catalase assay kit and total SOD assay kits (Beyotime, Shanghai, China). ..

peg catalase (Millipore)

Structured Review

Images

1) Product Images from "Enhanced Renal Afferent Arteriolar Reactive Oxygen Species and Contractility to Endothelin-1 Are Associated with Canonical Wnt Signaling in Diabetic Mice"

2) Product Images from "Restoration of afferent arteriolar autoregulatory behavior in ischemia-reperfusion injury in rat kidneys"

3) Product Images from "ÃÂ±1AMPK deletion in myelomonocytic cells induces a pro-inflammatory phenotype and enhances angiotensin II-induced vascular dysfunction"

4) Product Images from "BCR-ABL tyrosine kinase inhibitors promote pathological changes in dilator phenotype in the human microvasculature"

5) Product Images from "ÃÂ±1AMPK deletion in myelomonocytic cells induces a pro-inflammatory phenotype and enhances angiotensin II-induced vascular dysfunction"

6) Product Images from "Role of Mitochondrial Electron Transport Chain Complexes in Capsaicin Mediated Oxidative Stress Leading to Apoptosis in Pancreatic Cancer Cells"

7) Product Images from "The NADPH Oxidase Subunit p22phox Inhibits the Function of the Tumor Suppressor Protein Tuberin"

8) Product Images from "TLR4 signaling induces TLR2 expression in endothelial cells via neutrophil NADPH oxidase"

9) Product Images from "2-Deoxy-d-Glucose Combined with Cisplatin Enhances Cytotoxicity via Metabolic Oxidative Stress in Human Head and Neck Cancer Cells"

10) Product Images from "Release of cellular tension signals self-restorative ventral lamellipodia to heal barrier micro-wounds"

12) Product Images from "Chronic hypoxia limits H2O2-induced inhibition of ASIC1-dependent store-operated calcium entry in pulmonary arterial smooth muscle"

13) Product Images from "Role of ER Stress Response in Photodynamic Therapy: ROS Generated in Different Subcellular Compartments Trigger Diverse Cell Death Pathways"

14) Product Images from "Pressor Effect of Apelin-13 in the Rostral Ventrolateral Medulla: Role of NAD(P)H Oxidase-Derived Superoxide"

15) Product Images from "Platelet hyperaggregability in high-fat fed rats: A role for intraplatelet reactive-oxygen species production"

16) Product Images from "Reactive Oxygen Species Are Involved in Regulating Hypocontractility of Mesenteric Artery to Norepinephrine in Cirrhotic Rats with Portal Hypertension"

17) Product Images from "Enhanced Renal Afferent Arteriolar Reactive Oxygen Species and Contractility to Endothelin-1 Are Associated with Canonical Wnt Signaling in Diabetic Mice"

18) Product Images from "Hydrogen Peroxide Regulates Extracellular Superoxide Dismutase Activity and Expression in Neonatal Pulmonary Hypertension"

19) Product Images from "Juglanthraquinone C Induces Intracellular ROS Increase and Apoptosis by Activating the Akt/Foxo Signal Pathway in HCC Cells"

20) Product Images from "SIRT2 Interacts with β-catenin to Inhibit Wnt Signaling Output in Response to Radiation-Induced Stress"

21) Product Images from "Tumor Necrosis Factor–Related Apoptosis‐Inducing Ligand ( TRAIL) Promotes Angiogenesis and Ischemia‐Induced Neovascularization Via NADPH Oxidase 4 (NOX4) and Nitric Oxide–Dependent Mechanisms"