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  • 93
    RayBiotech mcp 1
    Summary diagram . TLR4 or TNFα receptor stimulation increases the activity of NF-κB and the expression of its target genes NR4A1–3 (NR4A), <t>MCP-1,</t> MIP-3α, and Relb. Loss of NR4A potentiates this induction of MCP-1, while reducing the induction of Relb and MIP-3α. Furthermore using mouse embryonic cells, we identify MIP-3α is a novel Relb target gene. Therefore, NR4A receptors act as repressors of inflammatory-NF-κB-driven MCP-1 (indicated by a red T bar) and enhancers of NF-κB-driven Relb and subsequently MIP-3α. Using a NR4A2 DNA-binding mutant reveals that NR4A2 does not require the ability to bind DNA in order to enhance/repress target genes simultaneously.
    Mcp 1, supplied by RayBiotech, used in various techniques. Bioz Stars score: 93/100, based on 265 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    mcp 1  (ATCC)
    91
    ATCC mcp 1
    CD44, LFA-1, MAC-1, VCAM-1, <t>MCP-1</t> and cathepsin B mRNA levels in 13 week old mouse blood leukocytes. Gene expression in blood leukocytes from 13 week old mice on a chow diet, all normalized to cyclophilin D and expressed as % change relative to wild type (KO: n = 22; TG: n = 12; WT: n = 11). TG is apoE −/− expressing low-level transgenic apoE, KO is apoE knockout, and WT is wild type. Leukocytes were prepared as described in Materials and Methods . The gene expression levels were not different between the groups for all the genes tested except for MCP1, which was significantly elevated in the KO and TG groups (Bonferroni test, *p
    Mcp 1, supplied by ATCC, used in various techniques. Bioz Stars score: 91/100, based on 55 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Cell Signaling Technology Inc mcp1
    Interplay between Ang II–induced inflammatory events in the heart triggered by cardiomyocyte CaMKIIδ. Cardiomyocyte CaMKIIδ is activated by Ang II infusion resulting in initiation of an early transcriptional proinflammatory gene program. This event contributes to recruitment of macrophages through <t>MCP1</t> and inflammasome activation, both of which produce a feed-forward proinflammatory signal that culminates with an outcome of cardiac fibrosis.
    Mcp1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 30 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    RayBiotech mcp 1 ccl2 elisa kits
    3α,5α-THP inhibits TLR4 signal innately activated in P rat VTA by blocking TLR4/α2 binding and TLR4/MyD88 binding. ( A ) 3α,5α-THP administration (15 mg/kg) significantly reduced <t>MCP-1</t> <t>(ELISA;</t> Student’s t(16) = 2.19), TRAF6 (Student’s t(16) = 5.74), and CRF (Student’s t(16) = 3.112) levels compared to vehicle controls, with no effect on TLR4 protein expression. *p
    Mcp 1 Ccl2 Elisa Kits, supplied by RayBiotech, used in various techniques. Bioz Stars score: 93/100, based on 231 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    RayBiotech a mouse specific mcp 1 elisa
    Late-life intervention with fisetin in aged wild-type mice extends health span and lifespan. (A) At 85-weeks of age ( > 20 mth), male and female mice were administered a diet containing 500 ppm (500 mg/kg) fisetin or fed a control diet with no drug. Lifespan was measured. n = 8–9 mice per group. Log rank (Mantel-Cox) test. (B) Median lifespan of the same cohort of mice. Each dot represents an individual animal. Black bars indicate the mean ± S.E.M. Two-tailed unpaired Student's t -test. (C) Clinical chemistry on blood from the above mice to measure markers of liver (alanine aminotransferase/ALT) and pancreatic (amylase/AMY) dysfunction. n = 3–6 mice per group. Two-tailed unpaired Student's t -test. (D) Composite lesion scores for aged-related pathologies in multiple tissues determined by histopathologic analysis according to the criteria of the Geropathology Grading Platform [ 63 ]. n = 3–8 mice per group. Two-tailed unpaired Student's t -test. (E) Representative images of the kidney of a mouse fed control chow or fisetin chow. In the control mouse, arrows (from left to right) indicate increased cellularity at a segment of the glomerular capsule border, moderate levels of lymphoid aggregates, and tubular cell vacuolization. In the fisetin-treated mouse, the arrow indicates only mild segmental cellularity at the glomerular capsule border and a few scattered lymphoid cells near the glomerulus (200× magnification). (F-I)—Tissues from > 120-week-old mice (~30 mth) fed control or fisetin chow were analyzed for the presence of senescence ( p16 Ink4a and p21 ) and senescence-associated secretory phenotype (SASP) ( Il1β , Il6 , Il10, Tnfα, Cxcl2 , Mcp1 , and Pai1 ) markers by qRT-PCR. Results are expressed as a function of values in 16–18-week-old “Young” WT mice. n = 4–10 mice per group. One-way ANOVA with Tukey's multiple comparison test. (J) Senescence and SASP marker expression were measured in CD3 + peripheral T cells by qRT-PCR. Results are expressed as a function of values in 16–18-week-old “Young” WT mice. n = 4–6 mice per group. One-way ANOVA with Tukey's multiple comparison test. (K) Circulating levels of the SASP factor chemokine <t>MCP-1</t> were measured by <t>ELISA.</t> n = 5 mice per group. One-way ANOVA with Tukey's multiple comparison test. (L) 4-hydroxynonenal (HNE) adducts a marker of lipid peroxidation and oxidative stress measured by ELISA in liver. n = 5–6 mice per group. Two-tailed unpaired Student's t -test. (M) The ratio of reduced (GSH) to oxidized (GSSG) glutathione was measured as an index oxidative stress. n = 6–7 mice per group. Values represented as the mean ± SEM. Two-tailed unpaired Student's t- test. *p
    A Mouse Specific Mcp 1 Elisa, supplied by RayBiotech, used in various techniques. Bioz Stars score: 93/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    RayBiotech human mcp 1 elisa kit
    SR141716A decreases the basal <t>MCP-1</t> secretion, and slightly the LPS-induced MCP-1 secretion in mature adipocytes . Adipocytes were treated with 1 μg/mL LPS and/or not with SR141716A from 50 to 400 nM. MCP-1 secretion was measured in media after 6 hours treatment by <t>ELISA.</t> Results are expressed in percentage, normalised to LPS (100% represents from 2 to 5 ng/mL MCP-1, depending on the patients). The graph shows the mean ± SD of the results from 3 patients (n = 6 for each condition, for each patient). **P
    Human Mcp 1 Elisa Kit, supplied by RayBiotech, used in various techniques. Bioz Stars score: 93/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    RayBiotech mcp 1 ccl2 elisa kit
    Figure 2A. Kegg Diagram interconnecting MAPK signaling with <t>CCL2</t> release. CCL2 release is initiated by TNFα acting on TNFR1 and contributes to leukocyte recruitment. The factors analyzed in this study are highlighted.
    Mcp 1 Ccl2 Elisa Kit, supplied by RayBiotech, used in various techniques. Bioz Stars score: 88/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Thermo Fisher mcp 1 hs00234140
    Figure 2A. Kegg Diagram interconnecting MAPK signaling with <t>CCL2</t> release. CCL2 release is initiated by TNFα acting on TNFR1 and contributes to leukocyte recruitment. The factors analyzed in this study are highlighted.
    Mcp 1 Hs00234140, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 88/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    95
    Cell Signaling Technology Inc anti mcp 1
    Effect of ANP on mRNA expression levels of IL-1β, TNF-α, <t>CCL2,</t> and CCR2 in the aorta. (A) mRNA expression levels of IL-1β, (B) mRNA expression levels of TNF-α, (C) mRNA expression levels of CCL2, (D) mRNA expression levels of CCR2. Compared with control group, # p
    Anti Mcp 1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 21 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    95
    Millipore mcp 1
    <t>MCP-1</t> induces intracellular calcium increase in DRG neurons following paclitaxel treatment
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    Image Search Results


    Summary diagram . TLR4 or TNFα receptor stimulation increases the activity of NF-κB and the expression of its target genes NR4A1–3 (NR4A), MCP-1, MIP-3α, and Relb. Loss of NR4A potentiates this induction of MCP-1, while reducing the induction of Relb and MIP-3α. Furthermore using mouse embryonic cells, we identify MIP-3α is a novel Relb target gene. Therefore, NR4A receptors act as repressors of inflammatory-NF-κB-driven MCP-1 (indicated by a red T bar) and enhancers of NF-κB-driven Relb and subsequently MIP-3α. Using a NR4A2 DNA-binding mutant reveals that NR4A2 does not require the ability to bind DNA in order to enhance/repress target genes simultaneously.

    Journal: Frontiers in Immunology

    Article Title: NR4A Receptors Differentially Regulate NF-κB Signaling in Myeloid Cells

    doi: 10.3389/fimmu.2017.00007

    Figure Lengend Snippet: Summary diagram . TLR4 or TNFα receptor stimulation increases the activity of NF-κB and the expression of its target genes NR4A1–3 (NR4A), MCP-1, MIP-3α, and Relb. Loss of NR4A potentiates this induction of MCP-1, while reducing the induction of Relb and MIP-3α. Furthermore using mouse embryonic cells, we identify MIP-3α is a novel Relb target gene. Therefore, NR4A receptors act as repressors of inflammatory-NF-κB-driven MCP-1 (indicated by a red T bar) and enhancers of NF-κB-driven Relb and subsequently MIP-3α. Using a NR4A2 DNA-binding mutant reveals that NR4A2 does not require the ability to bind DNA in order to enhance/repress target genes simultaneously.

    Article Snippet: Several studies have shown in both human and mouse macrophages, using NR4A1–3 overexpression and/or knockout cells, that NR4A receptors regulate expression of several downstream NF-κB target genes including IKKi, TNFα, MCP-1, iNos, IP-10, and IL-12 ( , , – ).

    Techniques: Activity Assay, Expressing, Activated Clotting Time Assay, Binding Assay, Mutagenesis

    NR4A2 and 3 negatively regulate TLR4 driven MCP-1 in human and murine myeloid cells . (A,B) Undifferentiated THP-1 cells transduced with shRNA directed against scrambled non-target control, NR4A2, or NR4A3 were treated with 1 µg/ml lipopolysaccharide (LPS) for 18 h (B) and 24 h (A) , followed by media collection and RNA isolation, respectively. (C) Undifferentiated THP-1 cells were pretreated with 10 µM NF-κB inhibitor (NF-κBi) for 1 h followed by the addition of 1 µg/ml LPS for 24 h, followed by media collection. (D) Murine raw mac 264.7 cells transduced with shRNA directed against scrambled non-target control and NR4A2 were exposed to LPS for 1 h. (E) Murine raw mac 264.7 cells transduced with shRNA directed against scrambled non-target control and NR4A2 were exposed to 1 µg/ml LPS for 2 h. (F) Murine raw mac 264.7 cells were pretreated with 10 µM NF-κB inhibitor (NF-κBi) for 1 h followed by exposure to 1 µg/ml LPS for 2 h. Analysis: ELISA analysis was performed for MCP-1 protein detection on media collected at times indicated (A,C) . RNA was isolated and RT-PCR was performed at indicated times to assess levels of MCP-1 NR4A2 and control gene GAPDH (B,D–F) . Un, untreated control. Data are expressed as fold over untreated control (FOC) or pg/ml ± SEM for n = minimum of three individual experiments. * p

    Journal: Frontiers in Immunology

    Article Title: NR4A Receptors Differentially Regulate NF-κB Signaling in Myeloid Cells

    doi: 10.3389/fimmu.2017.00007

    Figure Lengend Snippet: NR4A2 and 3 negatively regulate TLR4 driven MCP-1 in human and murine myeloid cells . (A,B) Undifferentiated THP-1 cells transduced with shRNA directed against scrambled non-target control, NR4A2, or NR4A3 were treated with 1 µg/ml lipopolysaccharide (LPS) for 18 h (B) and 24 h (A) , followed by media collection and RNA isolation, respectively. (C) Undifferentiated THP-1 cells were pretreated with 10 µM NF-κB inhibitor (NF-κBi) for 1 h followed by the addition of 1 µg/ml LPS for 24 h, followed by media collection. (D) Murine raw mac 264.7 cells transduced with shRNA directed against scrambled non-target control and NR4A2 were exposed to LPS for 1 h. (E) Murine raw mac 264.7 cells transduced with shRNA directed against scrambled non-target control and NR4A2 were exposed to 1 µg/ml LPS for 2 h. (F) Murine raw mac 264.7 cells were pretreated with 10 µM NF-κB inhibitor (NF-κBi) for 1 h followed by exposure to 1 µg/ml LPS for 2 h. Analysis: ELISA analysis was performed for MCP-1 protein detection on media collected at times indicated (A,C) . RNA was isolated and RT-PCR was performed at indicated times to assess levels of MCP-1 NR4A2 and control gene GAPDH (B,D–F) . Un, untreated control. Data are expressed as fold over untreated control (FOC) or pg/ml ± SEM for n = minimum of three individual experiments. * p

    Article Snippet: Several studies have shown in both human and mouse macrophages, using NR4A1–3 overexpression and/or knockout cells, that NR4A receptors regulate expression of several downstream NF-κB target genes including IKKi, TNFα, MCP-1, iNos, IP-10, and IL-12 ( , , – ).

    Techniques: Transduction, shRNA, Isolation, Enzyme-linked Immunosorbent Assay, Reverse Transcription Polymerase Chain Reaction

    CD44, LFA-1, MAC-1, VCAM-1, MCP-1 and cathepsin B mRNA levels in 13 week old mouse blood leukocytes. Gene expression in blood leukocytes from 13 week old mice on a chow diet, all normalized to cyclophilin D and expressed as % change relative to wild type (KO: n = 22; TG: n = 12; WT: n = 11). TG is apoE −/− expressing low-level transgenic apoE, KO is apoE knockout, and WT is wild type. Leukocytes were prepared as described in Materials and Methods . The gene expression levels were not different between the groups for all the genes tested except for MCP1, which was significantly elevated in the KO and TG groups (Bonferroni test, *p

    Journal: PLoS ONE

    Article Title: Altered Gene Expression in Early Atherosclerosis Is Blocked by Low Level Apolipoprotein E

    doi: 10.1371/journal.pone.0002503

    Figure Lengend Snippet: CD44, LFA-1, MAC-1, VCAM-1, MCP-1 and cathepsin B mRNA levels in 13 week old mouse blood leukocytes. Gene expression in blood leukocytes from 13 week old mice on a chow diet, all normalized to cyclophilin D and expressed as % change relative to wild type (KO: n = 22; TG: n = 12; WT: n = 11). TG is apoE −/− expressing low-level transgenic apoE, KO is apoE knockout, and WT is wild type. Leukocytes were prepared as described in Materials and Methods . The gene expression levels were not different between the groups for all the genes tested except for MCP1, which was significantly elevated in the KO and TG groups (Bonferroni test, *p

    Article Snippet: MCP-1 (Image clone ID; 5351355), LFA-1 (Image clone ID: 4015574), MAC-1 (Image clone ID: 3810731) and Cathepsin B (Image clone ID: 1887225) cDNA clones were purchased from ATCC. eNOS and CD44 clones were kindly provided by Dr. Philip A. Marsden's laboratory at the University of Toronto and Dr. Thomas P. St. John (ICOS Corporation) respectively.

    Techniques: Expressing, Mouse Assay, Transgenic Assay, Knock-Out

    Gene expression of CD44, LFA-1, MAC-1, VCAM-1, MCP-1, cathepsin B, eNOS, ICAM-1, and COX-2 in of older mice. A, gene expression in pooled aortic arches expressed as % change relative to wild type (KO: n = 10; TG: n = 10; WT: n = 5) from 8.5 mo old mice on chow diet, all normalized to cyclophilin D mRNA levels. TG is apoE −/− expressing low-level transgenic apoE, KO is apoE knockout, and WT is wild type. B, mRNA expression of adhesion molecules/cofactors in individual aortic arches (KO: n = 13; TG: n = 19, WT: n = 10) from 13 week old mice on a chow diet, normalized to cyclophilin D mRNA levels. CD44, LFA-1 and MAC-1 RNA levels were elevated in apoE −/− mice compared to wild type mice (Bonferroni test, *p

    Journal: PLoS ONE

    Article Title: Altered Gene Expression in Early Atherosclerosis Is Blocked by Low Level Apolipoprotein E

    doi: 10.1371/journal.pone.0002503

    Figure Lengend Snippet: Gene expression of CD44, LFA-1, MAC-1, VCAM-1, MCP-1, cathepsin B, eNOS, ICAM-1, and COX-2 in of older mice. A, gene expression in pooled aortic arches expressed as % change relative to wild type (KO: n = 10; TG: n = 10; WT: n = 5) from 8.5 mo old mice on chow diet, all normalized to cyclophilin D mRNA levels. TG is apoE −/− expressing low-level transgenic apoE, KO is apoE knockout, and WT is wild type. B, mRNA expression of adhesion molecules/cofactors in individual aortic arches (KO: n = 13; TG: n = 19, WT: n = 10) from 13 week old mice on a chow diet, normalized to cyclophilin D mRNA levels. CD44, LFA-1 and MAC-1 RNA levels were elevated in apoE −/− mice compared to wild type mice (Bonferroni test, *p

    Article Snippet: MCP-1 (Image clone ID; 5351355), LFA-1 (Image clone ID: 4015574), MAC-1 (Image clone ID: 3810731) and Cathepsin B (Image clone ID: 1887225) cDNA clones were purchased from ATCC. eNOS and CD44 clones were kindly provided by Dr. Philip A. Marsden's laboratory at the University of Toronto and Dr. Thomas P. St. John (ICOS Corporation) respectively.

    Techniques: Expressing, Mouse Assay, Transgenic Assay, Knock-Out

    Gene expression of CD44, LFA-1, MAC-1, VCAM-1, MCP-1, cathepsin B, eNOS, ICAM-1, and COX-2 in younger mice. Gene expression of CD44, LFA-1, MAC-1, VCAM-1, MCP-1, cathepsin B, eNOS, ICAM-1, and COX-2 in individual aortic arches expressed as % change relative to wild-type ( n = 8 for all groups) from 10- (A) week old mice. Data from 6- (B) week old mice are from pooled aortas, due to the small sample size. Both sets of mice were on chow diet and normalized to cyclophilin D mRNA levels. ApoE −/− mice had higher CD44, LFA-1, VCAM-1, cathepsin B, ICAM-1 and COX-2 gene expression than wild type mice (Bonferroni test, *p

    Journal: PLoS ONE

    Article Title: Altered Gene Expression in Early Atherosclerosis Is Blocked by Low Level Apolipoprotein E

    doi: 10.1371/journal.pone.0002503

    Figure Lengend Snippet: Gene expression of CD44, LFA-1, MAC-1, VCAM-1, MCP-1, cathepsin B, eNOS, ICAM-1, and COX-2 in younger mice. Gene expression of CD44, LFA-1, MAC-1, VCAM-1, MCP-1, cathepsin B, eNOS, ICAM-1, and COX-2 in individual aortic arches expressed as % change relative to wild-type ( n = 8 for all groups) from 10- (A) week old mice. Data from 6- (B) week old mice are from pooled aortas, due to the small sample size. Both sets of mice were on chow diet and normalized to cyclophilin D mRNA levels. ApoE −/− mice had higher CD44, LFA-1, VCAM-1, cathepsin B, ICAM-1 and COX-2 gene expression than wild type mice (Bonferroni test, *p

    Article Snippet: MCP-1 (Image clone ID; 5351355), LFA-1 (Image clone ID: 4015574), MAC-1 (Image clone ID: 3810731) and Cathepsin B (Image clone ID: 1887225) cDNA clones were purchased from ATCC. eNOS and CD44 clones were kindly provided by Dr. Philip A. Marsden's laboratory at the University of Toronto and Dr. Thomas P. St. John (ICOS Corporation) respectively.

    Techniques: Expressing, Mouse Assay

    Inhibition of palmitate-induced MCP-1 production by THP-1 cells. hAd consistently and dose dependently inhibits the MCP-1 release. THP-1 cells were pre-incubated with 10 pM to 1 µM hAd for 2 h and subsequently stimulated with 100 µM palmitate for 24 h. Two different batches of hAd were compared (upward- and downward-pointing triangles) with controls with (square) and without (circle) palmitate.

    Journal: PLoS ONE

    Article Title: Recombinant Adiponectin Does Not Lower Plasma Glucose in Animal Models of Type 2 Diabetes

    doi: 10.1371/journal.pone.0044270

    Figure Lengend Snippet: Inhibition of palmitate-induced MCP-1 production by THP-1 cells. hAd consistently and dose dependently inhibits the MCP-1 release. THP-1 cells were pre-incubated with 10 pM to 1 µM hAd for 2 h and subsequently stimulated with 100 µM palmitate for 24 h. Two different batches of hAd were compared (upward- and downward-pointing triangles) with controls with (square) and without (circle) palmitate.

    Article Snippet: MCP-1 Release from THP-1 Cells THP-1 cells (ATCC) were cultured as described by the supplier.

    Techniques: Inhibition, Incubation

    Renal mRNA expression of MCP-1 and iNOS is reduced by gliotoxin treatment. Top: The RNA from renal cortex of healthy control, untreated nephritic, and gliotoxin-treated rats was analyzed by RT-PCR (33 cycles) with specific primers for rat MCP-1, iNOS, and GAPDH as a control. Blot representative of four. After densitometry of MCP-1 and iNOS bands and correction by GAPDH, data are expressed as fold increases in relation to control. Each bar (▪, untreated nephritis; □, gliotoxin-treated) represents the mean ± SD of the total number of animals from each group (*, P

    Journal: The American Journal of Pathology

    Article Title: Nuclear Factor-?B Inhibitors as Potential Novel Anti-Inflammatory Agents for the Treatment of Immune Glomerulonephritis

    doi:

    Figure Lengend Snippet: Renal mRNA expression of MCP-1 and iNOS is reduced by gliotoxin treatment. Top: The RNA from renal cortex of healthy control, untreated nephritic, and gliotoxin-treated rats was analyzed by RT-PCR (33 cycles) with specific primers for rat MCP-1, iNOS, and GAPDH as a control. Blot representative of four. After densitometry of MCP-1 and iNOS bands and correction by GAPDH, data are expressed as fold increases in relation to control. Each bar (▪, untreated nephritis; □, gliotoxin-treated) represents the mean ± SD of the total number of animals from each group (*, P

    Article Snippet: In cultured cells, MCP-1 mRNA expression was analyzed by Northern blot using cDNA probes for human MCP-1 and 28S ribosomal RNA (JE/pGEM-hJE34 and HHCD07; ATCC).

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction

    Gliotoxin and parthenolide inhibit the mRNA expression of MCP-1 and iNOS in human MCs. A: Human MCs were pretreated with either gliotoxin or parthenolide (1 μg/ml), then washed and incubated with LPS/cytokines. The MCP-1 mRNA expression at 6 hours was analyzed by Northern blot. Relative amounts of mRNA were established in relation to 28S expression as fold increases versus control cells. B: The iNOS promoter activity was analyzed in human MCs transfected with piNOS-Luc and stimulated for 24 hours in medium alone (▪) or containing LPS/cytokines (□). Data of luciferase activity were normalized to Renilla activity and protein amounts, and are expressed as fold increases, compared with control. C: The NO production at 24 hours in medium alone (▪) or containing LPS/cytokines (□) was analyzed by measuring the absorbance of a fluorescent reaction. Data of nitrite production (nmol/mg protein) are mean ± SD of two to five experiments made in duplicate (*, P

    Journal: The American Journal of Pathology

    Article Title: Nuclear Factor-?B Inhibitors as Potential Novel Anti-Inflammatory Agents for the Treatment of Immune Glomerulonephritis

    doi:

    Figure Lengend Snippet: Gliotoxin and parthenolide inhibit the mRNA expression of MCP-1 and iNOS in human MCs. A: Human MCs were pretreated with either gliotoxin or parthenolide (1 μg/ml), then washed and incubated with LPS/cytokines. The MCP-1 mRNA expression at 6 hours was analyzed by Northern blot. Relative amounts of mRNA were established in relation to 28S expression as fold increases versus control cells. B: The iNOS promoter activity was analyzed in human MCs transfected with piNOS-Luc and stimulated for 24 hours in medium alone (▪) or containing LPS/cytokines (□). Data of luciferase activity were normalized to Renilla activity and protein amounts, and are expressed as fold increases, compared with control. C: The NO production at 24 hours in medium alone (▪) or containing LPS/cytokines (□) was analyzed by measuring the absorbance of a fluorescent reaction. Data of nitrite production (nmol/mg protein) are mean ± SD of two to five experiments made in duplicate (*, P

    Article Snippet: In cultured cells, MCP-1 mRNA expression was analyzed by Northern blot using cDNA probes for human MCP-1 and 28S ribosomal RNA (JE/pGEM-hJE34 and HHCD07; ATCC).

    Techniques: Expressing, Incubation, Northern Blot, Activity Assay, Transfection, Luciferase

    Interplay between Ang II–induced inflammatory events in the heart triggered by cardiomyocyte CaMKIIδ. Cardiomyocyte CaMKIIδ is activated by Ang II infusion resulting in initiation of an early transcriptional proinflammatory gene program. This event contributes to recruitment of macrophages through MCP1 and inflammasome activation, both of which produce a feed-forward proinflammatory signal that culminates with an outcome of cardiac fibrosis.

    Journal: JCI Insight

    Article Title: CaMKII δ-mediated inflammatory gene expression and inflammasome activation in cardiomyocytes initiate inflammation and induce fibrosis

    doi: 10.1172/jci.insight.97054

    Figure Lengend Snippet: Interplay between Ang II–induced inflammatory events in the heart triggered by cardiomyocyte CaMKIIδ. Cardiomyocyte CaMKIIδ is activated by Ang II infusion resulting in initiation of an early transcriptional proinflammatory gene program. This event contributes to recruitment of macrophages through MCP1 and inflammasome activation, both of which produce a feed-forward proinflammatory signal that culminates with an outcome of cardiac fibrosis.

    Article Snippet: Blots were blocked in 5% milk 1× Tris-buffered saline/Tween 20 (TBST) before incubation overnight at 4°C with 1:250 cleaved caspase-3 (Cell Signaling Technology, 9661), 1:1,000 GAPDH (Cell Signaling Technology, 2118), 1:1,000 lamin A/C (Cell Signaling Technology, 2032), 1:500 MCP1 (Cell Signaling Technology, 2029), 1:500 NLRP3 (Cell Signaling Technology, 15101), 1:1,000 P65 (Cell Signaling Technology, 8242), 1:1,000 RhoGDI (Cell Signaling Technology, 2564), and 1:5,000 CaMKIIδ (provided by Donald Bers Laboratory, UC Davis, Davis, California, USA).

    Techniques: Activation Assay

    Ang II–induced macrophage accumulation in the heart is attenuated by CaMKIIδ gene deletion in the cardiomyocyte, inhibition of NF-κB activation, and MCP1 receptor blockade. ( A ) Representative pictures of cardiac cryosections stained with antibody to the pan-macrophage marker CD68 taken from mice infused with saline (vehicle [Veh]) or Ang II (1.5 μg/kg/min) for 1 day ( n = 3–6/group). Mouse groups include Camk2d fl/fl control (CTL) mice, cardiomyocyte-specific CaMKIIδ KO (CKO) mice, control mice injected intraperitoneally with the inhibitor of NF-κB activation BMS-345541 (BMS), and control mice injected with the MCP1 receptor antagonist RS102895 (RS). CD68, green; DAPI, blue. Mice in the BMS group were injected with water (–) or 45 mg/kg of BMS-345541 (+) at 3 time points throughout the 1-day infusion. Doses and injection times were 30 mg/kg at time 0 hours of infusion, 15 mg/kg at time 5 hours, and 60 mg/kg at time 8 hours infused with. Mice in the RS group were injected intraperitoneally with 1:1 DMSO/water (–) or 10 mg/kg RS102895 every 6 hours for 24 hours (+). ( B ) Quantitation of CD68 staining in cryosections taken from control and CKO mice infused with saline or Ang II. ( C ) Quantitation of CD68 staining in cryosections taken from control mice infused with saline or Ang II and injected with water or BMS. ( D ) Quantitation of CD68 staining in cryosections taken from control mice infused with saline or Ang II and injected with 1:1 DMSO/water or RS102895. Two-way ANOVA was used for all comparisons. * P

    Journal: JCI Insight

    Article Title: CaMKII δ-mediated inflammatory gene expression and inflammasome activation in cardiomyocytes initiate inflammation and induce fibrosis

    doi: 10.1172/jci.insight.97054

    Figure Lengend Snippet: Ang II–induced macrophage accumulation in the heart is attenuated by CaMKIIδ gene deletion in the cardiomyocyte, inhibition of NF-κB activation, and MCP1 receptor blockade. ( A ) Representative pictures of cardiac cryosections stained with antibody to the pan-macrophage marker CD68 taken from mice infused with saline (vehicle [Veh]) or Ang II (1.5 μg/kg/min) for 1 day ( n = 3–6/group). Mouse groups include Camk2d fl/fl control (CTL) mice, cardiomyocyte-specific CaMKIIδ KO (CKO) mice, control mice injected intraperitoneally with the inhibitor of NF-κB activation BMS-345541 (BMS), and control mice injected with the MCP1 receptor antagonist RS102895 (RS). CD68, green; DAPI, blue. Mice in the BMS group were injected with water (–) or 45 mg/kg of BMS-345541 (+) at 3 time points throughout the 1-day infusion. Doses and injection times were 30 mg/kg at time 0 hours of infusion, 15 mg/kg at time 5 hours, and 60 mg/kg at time 8 hours infused with. Mice in the RS group were injected intraperitoneally with 1:1 DMSO/water (–) or 10 mg/kg RS102895 every 6 hours for 24 hours (+). ( B ) Quantitation of CD68 staining in cryosections taken from control and CKO mice infused with saline or Ang II. ( C ) Quantitation of CD68 staining in cryosections taken from control mice infused with saline or Ang II and injected with water or BMS. ( D ) Quantitation of CD68 staining in cryosections taken from control mice infused with saline or Ang II and injected with 1:1 DMSO/water or RS102895. Two-way ANOVA was used for all comparisons. * P

    Article Snippet: Blots were blocked in 5% milk 1× Tris-buffered saline/Tween 20 (TBST) before incubation overnight at 4°C with 1:250 cleaved caspase-3 (Cell Signaling Technology, 9661), 1:1,000 GAPDH (Cell Signaling Technology, 2118), 1:1,000 lamin A/C (Cell Signaling Technology, 2032), 1:500 MCP1 (Cell Signaling Technology, 2029), 1:500 NLRP3 (Cell Signaling Technology, 15101), 1:1,000 P65 (Cell Signaling Technology, 8242), 1:1,000 RhoGDI (Cell Signaling Technology, 2564), and 1:5,000 CaMKIIδ (provided by Donald Bers Laboratory, UC Davis, Davis, California, USA).

    Techniques: Inhibition, Activation Assay, Staining, Marker, Mouse Assay, CTL Assay, Injection, Quantitation Assay

    Deletion of CaMKIIδ in the cardiomyocyte attenuates Ang II–induced inflammatory gene expression in the heart and monocyte chemotactic protein 1 expression in the myocyte. ( A ) mRNA expression of monocyte chemoattractant protein 1 ( Ccl2 /MCP1), macrophage inflammatory protein 1α ( Ccl3 /MIP1α), CXC motif ligand 1 ( Cxcl1 ), CXC motif ligand 2 ( Cxcl2 ),IL-1β ( Il1b ), and IL-6 ( Il6 ) in ventricular lysates of Camk2d fl/fl control (CTL) and cardiomyocyte-specific CaMKIIδ KO (CKO) mice infused with saline (vehicle [Veh]) or Ang II (1.5 μg/kg/min) for 1 day as measured by qPCR ( n = 6–9/group). ( B ) Ccl2/ MCP1 mRNA expression in adult mouse ventricular myocytes isolated from control and CKO mice after 1-day saline or Ang II infusion as measured by qPCR. Hearts were enzymatically digested, and resultant cell suspension was allowed to sediment by gravity. Supernatant was aspirated and pellet washed 2 times before being processed for RNA extraction, cDNA synthesis, and qPCR ( n = 3/group). ( C ) Western blot and quantitation of MCP1 protein in ventricular lysates of control and CKO mice at 1 day of Ang II infusion. GAPDH, loading control ( n = 4/group). Two-way ANOVA was used for all comparisons. * P

    Journal: JCI Insight

    Article Title: CaMKII δ-mediated inflammatory gene expression and inflammasome activation in cardiomyocytes initiate inflammation and induce fibrosis

    doi: 10.1172/jci.insight.97054

    Figure Lengend Snippet: Deletion of CaMKIIδ in the cardiomyocyte attenuates Ang II–induced inflammatory gene expression in the heart and monocyte chemotactic protein 1 expression in the myocyte. ( A ) mRNA expression of monocyte chemoattractant protein 1 ( Ccl2 /MCP1), macrophage inflammatory protein 1α ( Ccl3 /MIP1α), CXC motif ligand 1 ( Cxcl1 ), CXC motif ligand 2 ( Cxcl2 ),IL-1β ( Il1b ), and IL-6 ( Il6 ) in ventricular lysates of Camk2d fl/fl control (CTL) and cardiomyocyte-specific CaMKIIδ KO (CKO) mice infused with saline (vehicle [Veh]) or Ang II (1.5 μg/kg/min) for 1 day as measured by qPCR ( n = 6–9/group). ( B ) Ccl2/ MCP1 mRNA expression in adult mouse ventricular myocytes isolated from control and CKO mice after 1-day saline or Ang II infusion as measured by qPCR. Hearts were enzymatically digested, and resultant cell suspension was allowed to sediment by gravity. Supernatant was aspirated and pellet washed 2 times before being processed for RNA extraction, cDNA synthesis, and qPCR ( n = 3/group). ( C ) Western blot and quantitation of MCP1 protein in ventricular lysates of control and CKO mice at 1 day of Ang II infusion. GAPDH, loading control ( n = 4/group). Two-way ANOVA was used for all comparisons. * P

    Article Snippet: Blots were blocked in 5% milk 1× Tris-buffered saline/Tween 20 (TBST) before incubation overnight at 4°C with 1:250 cleaved caspase-3 (Cell Signaling Technology, 9661), 1:1,000 GAPDH (Cell Signaling Technology, 2118), 1:1,000 lamin A/C (Cell Signaling Technology, 2032), 1:500 MCP1 (Cell Signaling Technology, 2029), 1:500 NLRP3 (Cell Signaling Technology, 15101), 1:1,000 P65 (Cell Signaling Technology, 8242), 1:1,000 RhoGDI (Cell Signaling Technology, 2564), and 1:5,000 CaMKIIδ (provided by Donald Bers Laboratory, UC Davis, Davis, California, USA).

    Techniques: Expressing, CTL Assay, Mouse Assay, Real-time Polymerase Chain Reaction, Isolation, RNA Extraction, Western Blot, Quantitation Assay

    Inhibition of MCP1 or inflammasome signaling attenuates cardiac fibrosis induced by Ang II infusion. Camk2d fl/fl control mice were injected intraperitoneally with either 10 mg/kg RS102895 (RS) every 6 hours ( A and B ) or 10 mg/kg MCC950 (MCC) every 12 hours ( C and D ) starting 1 hour prior to a 3-day saline (vehicle [Veh]) or Ang II (1.5 μg/kg/min) infusion (inf). ( A ) Representative pictures and quantitation of paraffin-embedded sections stained with Masson’s trichrome ( n = 3–6/group). ( B ) mRNA expression of fibrotic markers collagen 1α1 ( Col1a1 ), collagen 3α1 ( Col3a1 ), and periostin ( Postn ) in ventricles as measured by qPCR ( n = 3–6/group). ( C ) Representative pictures of paraffin-embedded sections stained with Masson’s trichrome ( n = 3–4/group). ( D ) mRNA expression of fibrotic markers Col1a1 , Col3a1 , and Postn in ventricles as measured by qPCR ( n = 3–6/group). Two-way ANOVA was used for all comparisons. * P

    Journal: JCI Insight

    Article Title: CaMKII δ-mediated inflammatory gene expression and inflammasome activation in cardiomyocytes initiate inflammation and induce fibrosis

    doi: 10.1172/jci.insight.97054

    Figure Lengend Snippet: Inhibition of MCP1 or inflammasome signaling attenuates cardiac fibrosis induced by Ang II infusion. Camk2d fl/fl control mice were injected intraperitoneally with either 10 mg/kg RS102895 (RS) every 6 hours ( A and B ) or 10 mg/kg MCC950 (MCC) every 12 hours ( C and D ) starting 1 hour prior to a 3-day saline (vehicle [Veh]) or Ang II (1.5 μg/kg/min) infusion (inf). ( A ) Representative pictures and quantitation of paraffin-embedded sections stained with Masson’s trichrome ( n = 3–6/group). ( B ) mRNA expression of fibrotic markers collagen 1α1 ( Col1a1 ), collagen 3α1 ( Col3a1 ), and periostin ( Postn ) in ventricles as measured by qPCR ( n = 3–6/group). ( C ) Representative pictures of paraffin-embedded sections stained with Masson’s trichrome ( n = 3–4/group). ( D ) mRNA expression of fibrotic markers Col1a1 , Col3a1 , and Postn in ventricles as measured by qPCR ( n = 3–6/group). Two-way ANOVA was used for all comparisons. * P

    Article Snippet: Blots were blocked in 5% milk 1× Tris-buffered saline/Tween 20 (TBST) before incubation overnight at 4°C with 1:250 cleaved caspase-3 (Cell Signaling Technology, 9661), 1:1,000 GAPDH (Cell Signaling Technology, 2118), 1:1,000 lamin A/C (Cell Signaling Technology, 2032), 1:500 MCP1 (Cell Signaling Technology, 2029), 1:500 NLRP3 (Cell Signaling Technology, 15101), 1:1,000 P65 (Cell Signaling Technology, 8242), 1:1,000 RhoGDI (Cell Signaling Technology, 2564), and 1:5,000 CaMKIIδ (provided by Donald Bers Laboratory, UC Davis, Davis, California, USA).

    Techniques: Inhibition, Mouse Assay, Injection, Quantitation Assay, Staining, Expressing, Real-time Polymerase Chain Reaction

    MPs are released by stressed adipocytes in a caspase 3 and Rho-associated kinase dependent manner. (A-D) Characterization of adipocyte-derived MPs. (A) Morphology of the differentiated 3T3-L1 adipocytes treated with control, 0.5 mM palmitic acid. (B) The number of Annexin V positive MPs was quantitated by flow cytometry. (C) Dynamic light scattering analysis and Transmission Electron Microscopy of isolated MPs. Isolated MPs were measured by Zetasizer and analyzed using intensity. (D) Western Blot analysis of MPs released by adipocytes. Isolated MPs were fractionated by SDS-PAGE and probed with FABP4, MCP-1, Chemerin, Adiponectin and Perilipin antibody. (E-F) Differentiated adipocytes were incubated with or without palmitic acid in the absence or presence of a selective caspase-3 inhibitor (E), or a range of doses of two different Rho associated kinase inhibitors (Y27632 and fasudil) (F) for up to 12 hrs. Supernatants were then collected and MPs isolated by ultracentrifugation as detailed in methods section. (G) Morphology of isolated mouse primary adipocytes. (H) Number of annexin V positive mouse primary adipocyte-derived MPs assessed by flow cytometry. Values represent mean ± S.D. * P

    Journal: PLoS ONE

    Article Title: Microparticles Release by Adipocytes Act as “Find-Me” Signals to Promote Macrophage Migration

    doi: 10.1371/journal.pone.0123110

    Figure Lengend Snippet: MPs are released by stressed adipocytes in a caspase 3 and Rho-associated kinase dependent manner. (A-D) Characterization of adipocyte-derived MPs. (A) Morphology of the differentiated 3T3-L1 adipocytes treated with control, 0.5 mM palmitic acid. (B) The number of Annexin V positive MPs was quantitated by flow cytometry. (C) Dynamic light scattering analysis and Transmission Electron Microscopy of isolated MPs. Isolated MPs were measured by Zetasizer and analyzed using intensity. (D) Western Blot analysis of MPs released by adipocytes. Isolated MPs were fractionated by SDS-PAGE and probed with FABP4, MCP-1, Chemerin, Adiponectin and Perilipin antibody. (E-F) Differentiated adipocytes were incubated with or without palmitic acid in the absence or presence of a selective caspase-3 inhibitor (E), or a range of doses of two different Rho associated kinase inhibitors (Y27632 and fasudil) (F) for up to 12 hrs. Supernatants were then collected and MPs isolated by ultracentrifugation as detailed in methods section. (G) Morphology of isolated mouse primary adipocytes. (H) Number of annexin V positive mouse primary adipocyte-derived MPs assessed by flow cytometry. Values represent mean ± S.D. * P

    Article Snippet: Macrophages, that infiltrate the adipose tissue of obese mice and humans, are the major source for some of these products, especially of pro-inflammatory cytokines such as TNF-alpha and IL-6 and chemokines such as MCP-1 [ – , ].

    Techniques: Derivative Assay, Flow Cytometry, Cytometry, Transmission Assay, Electron Microscopy, Isolation, Western Blot, SDS Page, Incubation

    Attraction of monocytes and macrophages to supernatants of mature adipocytes exposed to palmitic acid. Migration of (A) RAW264.7 cells or (B) primary mouse macrophages through a transwell (8 μm pore size) to supernatants from untreated (control) or treated differentiated mature adipocytes with 0.5mM palmitic acid. MCP-1 (50 ng/ml) was used as positive control. (C) Adipocytes were treated with 0.5 mM palmitic acid in the absence or presence of 0.025 U/ml apyrase, 0.5 U/ml phospholipase-D or 50 μg/ml control IgG or MCP-1 neutralizing antibody. Macrophages that migrated to the lower chamber were stained with DAPI and the number of cells was counted under fluorescence microscopy. Values represent as mean ± S.D. of representative experiment. * P

    Journal: PLoS ONE

    Article Title: Microparticles Release by Adipocytes Act as “Find-Me” Signals to Promote Macrophage Migration

    doi: 10.1371/journal.pone.0123110

    Figure Lengend Snippet: Attraction of monocytes and macrophages to supernatants of mature adipocytes exposed to palmitic acid. Migration of (A) RAW264.7 cells or (B) primary mouse macrophages through a transwell (8 μm pore size) to supernatants from untreated (control) or treated differentiated mature adipocytes with 0.5mM palmitic acid. MCP-1 (50 ng/ml) was used as positive control. (C) Adipocytes were treated with 0.5 mM palmitic acid in the absence or presence of 0.025 U/ml apyrase, 0.5 U/ml phospholipase-D or 50 μg/ml control IgG or MCP-1 neutralizing antibody. Macrophages that migrated to the lower chamber were stained with DAPI and the number of cells was counted under fluorescence microscopy. Values represent as mean ± S.D. of representative experiment. * P

    Article Snippet: Macrophages, that infiltrate the adipose tissue of obese mice and humans, are the major source for some of these products, especially of pro-inflammatory cytokines such as TNF-alpha and IL-6 and chemokines such as MCP-1 [ – , ].

    Techniques: Migration, Positive Control, Staining, Fluorescence, Microscopy

    LV MMP-9 and MCP-1 levels correlate with each other and their corresponding plasma concentrations. (A) A graph showing LV MMP-9 levels correlate with plasma MMP-9 concentrations by Spearman's rank correlation. (B) A graph showing LV MCP-1 levels correlate

    Journal: Circulation. Cardiovascular genetics

    Article Title: Multi-analyte Profiling Reveals MMP-9 and MCP-1 as Plasma Biomarkers of Cardiac Aging

    doi: 10.1161/CIRCGENETICS.111.959981

    Figure Lengend Snippet: LV MMP-9 and MCP-1 levels correlate with each other and their corresponding plasma concentrations. (A) A graph showing LV MMP-9 levels correlate with plasma MMP-9 concentrations by Spearman's rank correlation. (B) A graph showing LV MCP-1 levels correlate

    Article Snippet: The membrane was incubated with 5% blotting grade blocker non-fat dry milk (Bio-Rad) in 1X PBS (Sigma) for 1 hr at room temperature, followed by incubation with MMP-9 antibody (Abcam ab38898 at 1:5000 dilution), MCP-1 antibody (Cell signaling #2029 at 1:1000 dilution), or cleaved caspase-3 antibody (Cell signaling #9661 at 1:1000 dilution) for overnight at 4°C.

    Techniques:

    Plasma MMP-9 and MCP-1 Levels Correlated with End Diastolic Dimensions

    Journal: Circulation. Cardiovascular genetics

    Article Title: Multi-analyte Profiling Reveals MMP-9 and MCP-1 as Plasma Biomarkers of Cardiac Aging

    doi: 10.1161/CIRCGENETICS.111.959981

    Figure Lengend Snippet: Plasma MMP-9 and MCP-1 Levels Correlated with End Diastolic Dimensions

    Article Snippet: The membrane was incubated with 5% blotting grade blocker non-fat dry milk (Bio-Rad) in 1X PBS (Sigma) for 1 hr at room temperature, followed by incubation with MMP-9 antibody (Abcam ab38898 at 1:5000 dilution), MCP-1 antibody (Cell signaling #2029 at 1:1000 dilution), or cleaved caspase-3 antibody (Cell signaling #9661 at 1:1000 dilution) for overnight at 4°C.

    Techniques:

    MMP-9 and MCP-1 levels increase in the LV with senescence. (A) Immunoblot (upper panel) showing MMP-9 levels are significantly higher in the senescent LV compared to adult LV and corresponding densitometry results (lower panel). (B) Immunoblot (upper

    Journal: Circulation. Cardiovascular genetics

    Article Title: Multi-analyte Profiling Reveals MMP-9 and MCP-1 as Plasma Biomarkers of Cardiac Aging

    doi: 10.1161/CIRCGENETICS.111.959981

    Figure Lengend Snippet: MMP-9 and MCP-1 levels increase in the LV with senescence. (A) Immunoblot (upper panel) showing MMP-9 levels are significantly higher in the senescent LV compared to adult LV and corresponding densitometry results (lower panel). (B) Immunoblot (upper

    Article Snippet: The membrane was incubated with 5% blotting grade blocker non-fat dry milk (Bio-Rad) in 1X PBS (Sigma) for 1 hr at room temperature, followed by incubation with MMP-9 antibody (Abcam ab38898 at 1:5000 dilution), MCP-1 antibody (Cell signaling #2029 at 1:1000 dilution), or cleaved caspase-3 antibody (Cell signaling #9661 at 1:1000 dilution) for overnight at 4°C.

    Techniques:

    Plasma Multi-analyte Profiling Revealed Increased MMP-9 and MCP-1 Levels with Senescence

    Journal: Circulation. Cardiovascular genetics

    Article Title: Multi-analyte Profiling Reveals MMP-9 and MCP-1 as Plasma Biomarkers of Cardiac Aging

    doi: 10.1161/CIRCGENETICS.111.959981

    Figure Lengend Snippet: Plasma Multi-analyte Profiling Revealed Increased MMP-9 and MCP-1 Levels with Senescence

    Article Snippet: The membrane was incubated with 5% blotting grade blocker non-fat dry milk (Bio-Rad) in 1X PBS (Sigma) for 1 hr at room temperature, followed by incubation with MMP-9 antibody (Abcam ab38898 at 1:5000 dilution), MCP-1 antibody (Cell signaling #2029 at 1:1000 dilution), or cleaved caspase-3 antibody (Cell signaling #9661 at 1:1000 dilution) for overnight at 4°C.

    Techniques:

    3α,5α-THP inhibits TLR4 signal innately activated in P rat VTA by blocking TLR4/α2 binding and TLR4/MyD88 binding. ( A ) 3α,5α-THP administration (15 mg/kg) significantly reduced MCP-1 (ELISA; Student’s t(16) = 2.19), TRAF6 (Student’s t(16) = 5.74), and CRF (Student’s t(16) = 3.112) levels compared to vehicle controls, with no effect on TLR4 protein expression. *p

    Journal: Scientific Reports

    Article Title: Endogenous Neurosteroid (3α,5α)3-Hydroxypregnan-20-one Inhibits Toll-like-4 Receptor Activation and Pro-inflammatory Signaling in Macrophages and Brain

    doi: 10.1038/s41598-018-37409-6

    Figure Lengend Snippet: 3α,5α-THP inhibits TLR4 signal innately activated in P rat VTA by blocking TLR4/α2 binding and TLR4/MyD88 binding. ( A ) 3α,5α-THP administration (15 mg/kg) significantly reduced MCP-1 (ELISA; Student’s t(16) = 2.19), TRAF6 (Student’s t(16) = 5.74), and CRF (Student’s t(16) = 3.112) levels compared to vehicle controls, with no effect on TLR4 protein expression. *p

    Article Snippet: VTA micropunches were lysed with CelLyte MT and the extracts were assayed for protein content by the BCA procedure (Pierce) and for MCP-1 using the rat MCP-1 ELISA kit (Raybiotech, Cat. #ERC-MCP-1-CL; Norcross, GA, USA) as per manufacturer’s instructions.

    Techniques: Blocking Assay, Binding Assay, Enzyme-linked Immunosorbent Assay, Expressing

    Late-life intervention with fisetin in aged wild-type mice extends health span and lifespan. (A) At 85-weeks of age ( > 20 mth), male and female mice were administered a diet containing 500 ppm (500 mg/kg) fisetin or fed a control diet with no drug. Lifespan was measured. n = 8–9 mice per group. Log rank (Mantel-Cox) test. (B) Median lifespan of the same cohort of mice. Each dot represents an individual animal. Black bars indicate the mean ± S.E.M. Two-tailed unpaired Student's t -test. (C) Clinical chemistry on blood from the above mice to measure markers of liver (alanine aminotransferase/ALT) and pancreatic (amylase/AMY) dysfunction. n = 3–6 mice per group. Two-tailed unpaired Student's t -test. (D) Composite lesion scores for aged-related pathologies in multiple tissues determined by histopathologic analysis according to the criteria of the Geropathology Grading Platform [ 63 ]. n = 3–8 mice per group. Two-tailed unpaired Student's t -test. (E) Representative images of the kidney of a mouse fed control chow or fisetin chow. In the control mouse, arrows (from left to right) indicate increased cellularity at a segment of the glomerular capsule border, moderate levels of lymphoid aggregates, and tubular cell vacuolization. In the fisetin-treated mouse, the arrow indicates only mild segmental cellularity at the glomerular capsule border and a few scattered lymphoid cells near the glomerulus (200× magnification). (F-I)—Tissues from > 120-week-old mice (~30 mth) fed control or fisetin chow were analyzed for the presence of senescence ( p16 Ink4a and p21 ) and senescence-associated secretory phenotype (SASP) ( Il1β , Il6 , Il10, Tnfα, Cxcl2 , Mcp1 , and Pai1 ) markers by qRT-PCR. Results are expressed as a function of values in 16–18-week-old “Young” WT mice. n = 4–10 mice per group. One-way ANOVA with Tukey's multiple comparison test. (J) Senescence and SASP marker expression were measured in CD3 + peripheral T cells by qRT-PCR. Results are expressed as a function of values in 16–18-week-old “Young” WT mice. n = 4–6 mice per group. One-way ANOVA with Tukey's multiple comparison test. (K) Circulating levels of the SASP factor chemokine MCP-1 were measured by ELISA. n = 5 mice per group. One-way ANOVA with Tukey's multiple comparison test. (L) 4-hydroxynonenal (HNE) adducts a marker of lipid peroxidation and oxidative stress measured by ELISA in liver. n = 5–6 mice per group. Two-tailed unpaired Student's t -test. (M) The ratio of reduced (GSH) to oxidized (GSSG) glutathione was measured as an index oxidative stress. n = 6–7 mice per group. Values represented as the mean ± SEM. Two-tailed unpaired Student's t- test. *p

    Journal: EBioMedicine

    Article Title: Fisetin is a senotherapeutic that extends health and lifespan

    doi: 10.1016/j.ebiom.2018.09.015

    Figure Lengend Snippet: Late-life intervention with fisetin in aged wild-type mice extends health span and lifespan. (A) At 85-weeks of age ( > 20 mth), male and female mice were administered a diet containing 500 ppm (500 mg/kg) fisetin or fed a control diet with no drug. Lifespan was measured. n = 8–9 mice per group. Log rank (Mantel-Cox) test. (B) Median lifespan of the same cohort of mice. Each dot represents an individual animal. Black bars indicate the mean ± S.E.M. Two-tailed unpaired Student's t -test. (C) Clinical chemistry on blood from the above mice to measure markers of liver (alanine aminotransferase/ALT) and pancreatic (amylase/AMY) dysfunction. n = 3–6 mice per group. Two-tailed unpaired Student's t -test. (D) Composite lesion scores for aged-related pathologies in multiple tissues determined by histopathologic analysis according to the criteria of the Geropathology Grading Platform [ 63 ]. n = 3–8 mice per group. Two-tailed unpaired Student's t -test. (E) Representative images of the kidney of a mouse fed control chow or fisetin chow. In the control mouse, arrows (from left to right) indicate increased cellularity at a segment of the glomerular capsule border, moderate levels of lymphoid aggregates, and tubular cell vacuolization. In the fisetin-treated mouse, the arrow indicates only mild segmental cellularity at the glomerular capsule border and a few scattered lymphoid cells near the glomerulus (200× magnification). (F-I)—Tissues from > 120-week-old mice (~30 mth) fed control or fisetin chow were analyzed for the presence of senescence ( p16 Ink4a and p21 ) and senescence-associated secretory phenotype (SASP) ( Il1β , Il6 , Il10, Tnfα, Cxcl2 , Mcp1 , and Pai1 ) markers by qRT-PCR. Results are expressed as a function of values in 16–18-week-old “Young” WT mice. n = 4–10 mice per group. One-way ANOVA with Tukey's multiple comparison test. (J) Senescence and SASP marker expression were measured in CD3 + peripheral T cells by qRT-PCR. Results are expressed as a function of values in 16–18-week-old “Young” WT mice. n = 4–6 mice per group. One-way ANOVA with Tukey's multiple comparison test. (K) Circulating levels of the SASP factor chemokine MCP-1 were measured by ELISA. n = 5 mice per group. One-way ANOVA with Tukey's multiple comparison test. (L) 4-hydroxynonenal (HNE) adducts a marker of lipid peroxidation and oxidative stress measured by ELISA in liver. n = 5–6 mice per group. Two-tailed unpaired Student's t -test. (M) The ratio of reduced (GSH) to oxidized (GSSG) glutathione was measured as an index oxidative stress. n = 6–7 mice per group. Values represented as the mean ± SEM. Two-tailed unpaired Student's t- test. *p

    Article Snippet: 2.9 Serum MCP-1 Serum concentrations of MCP-1 (n = 5 mice per group) were measured using a mouse-specific MCP-1 ELISA (Raybiotech, Norcross, GA), as described [ ].

    Techniques: Mouse Assay, Two Tailed Test, Quantitative RT-PCR, Marker, Expressing, Enzyme-linked Immunosorbent Assay

    The CCL2/CCR2 pathway mediates the migration of SSC low CD11b + Gr1 dim cells to the NAFLD liver. (A) CCL2 expression in the livers of ND and HFD-fed mice was investigated by real-time RT-PCR (n = 5). (B, C) Protein expression of CCL2 in the livers was investigated by ELISA (B) (n = 5) and immunohistochemistry (C). Scale bars, 100 μm. (D) CCL2 gene expression in Hepa1-6 cells treated with oleic acid or palmitic acid analyzed by real-time RT-PCR (n = 5). (E) Migration assays revealed that SSC low CD11b + Gr1 dim cells migrated in response to CCL2 in vitro (n = 5). * P

    Journal: PLoS ONE

    Article Title: Characterization of Liver Monocytic Myeloid-Derived Suppressor Cells and Their Role in a Murine Model of Non-Alcoholic Fatty Liver Disease

    doi: 10.1371/journal.pone.0149948

    Figure Lengend Snippet: The CCL2/CCR2 pathway mediates the migration of SSC low CD11b + Gr1 dim cells to the NAFLD liver. (A) CCL2 expression in the livers of ND and HFD-fed mice was investigated by real-time RT-PCR (n = 5). (B, C) Protein expression of CCL2 in the livers was investigated by ELISA (B) (n = 5) and immunohistochemistry (C). Scale bars, 100 μm. (D) CCL2 gene expression in Hepa1-6 cells treated with oleic acid or palmitic acid analyzed by real-time RT-PCR (n = 5). (E) Migration assays revealed that SSC low CD11b + Gr1 dim cells migrated in response to CCL2 in vitro (n = 5). * P

    Article Snippet: CCL2 expression was investigated with a RayBio Mouse CCL2 ELISA Kit (RayBiotech, Norcross, GA, USA) according to the manufacturer's protocol.

    Techniques: Migration, Expressing, Mouse Assay, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Immunohistochemistry, In Vitro

    SR141716A decreases the basal MCP-1 secretion, and slightly the LPS-induced MCP-1 secretion in mature adipocytes . Adipocytes were treated with 1 μg/mL LPS and/or not with SR141716A from 50 to 400 nM. MCP-1 secretion was measured in media after 6 hours treatment by ELISA. Results are expressed in percentage, normalised to LPS (100% represents from 2 to 5 ng/mL MCP-1, depending on the patients). The graph shows the mean ± SD of the results from 3 patients (n = 6 for each condition, for each patient). **P

    Journal: Journal of Inflammation (London, England)

    Article Title: Effect of the Cannabinoid Receptor-1 antagonist SR141716A on human adipocyte inflammatory profile and differentiation

    doi: 10.1186/1476-9255-8-33

    Figure Lengend Snippet: SR141716A decreases the basal MCP-1 secretion, and slightly the LPS-induced MCP-1 secretion in mature adipocytes . Adipocytes were treated with 1 μg/mL LPS and/or not with SR141716A from 50 to 400 nM. MCP-1 secretion was measured in media after 6 hours treatment by ELISA. Results are expressed in percentage, normalised to LPS (100% represents from 2 to 5 ng/mL MCP-1, depending on the patients). The graph shows the mean ± SD of the results from 3 patients (n = 6 for each condition, for each patient). **P

    Article Snippet: ELISA assays for TNF-a, IL-6 and MCP-1 Following LPS stimulation for 6 hours, with or without SR141716A, media were assayed for TNF-a, IL-6 content with Ready-SET-Go human ELISA kits (eBioscience, Cliniscience, Montrouge, France), and for MCP-1 content with RayBio human MCP-1 ELISA kit (RayBioTech, Clinisciences, France), according to the manufacturer's instructions.

    Techniques: Enzyme-linked Immunosorbent Assay

    Figure 2A. Kegg Diagram interconnecting MAPK signaling with CCL2 release. CCL2 release is initiated by TNFα acting on TNFR1 and contributes to leukocyte recruitment. The factors analyzed in this study are highlighted.

    Journal: Cytokine

    Article Title: Diallyl disulfide inhibits TNFα induced CCL2 release through MAPK/ERK and NF-Kappa-B Signaling

    doi: 10.1016/j.cyto.2014.12.007

    Figure Lengend Snippet: Figure 2A. Kegg Diagram interconnecting MAPK signaling with CCL2 release. CCL2 release is initiated by TNFα acting on TNFR1 and contributes to leukocyte recruitment. The factors analyzed in this study are highlighted.

    Article Snippet: Specific ELISA was performed using MCP-1/CCL2 ELISA kit (Raybiotech, Norcross, GA, USA) following manufacturer’s instructions.

    Techniques:

    Time course of the TNFα-dependent accumulation of CCL2 in MDA-MB-231 cells

    Journal: Cytokine

    Article Title: Diallyl disulfide inhibits TNFα induced CCL2 release through MAPK/ERK and NF-Kappa-B Signaling

    doi: 10.1016/j.cyto.2014.12.007

    Figure Lengend Snippet: Time course of the TNFα-dependent accumulation of CCL2 in MDA-MB-231 cells

    Article Snippet: Specific ELISA was performed using MCP-1/CCL2 ELISA kit (Raybiotech, Norcross, GA, USA) following manufacturer’s instructions.

    Techniques: Multiple Displacement Amplification

    Effect of ANP on mRNA expression levels of IL-1β, TNF-α, CCL2, and CCR2 in the aorta. (A) mRNA expression levels of IL-1β, (B) mRNA expression levels of TNF-α, (C) mRNA expression levels of CCL2, (D) mRNA expression levels of CCR2. Compared with control group, # p

    Journal: Frontiers in Pharmacology

    Article Title: Anti-Atherosclerosis Effect of Angong Niuhuang Pill via Regulating Th17/Treg Immune Balance and Inhibiting Chronic Inflammatory on ApoE-/- Mice Model of Early and Mid-Term Atherosclerosis

    doi: 10.3389/fphar.2019.01584

    Figure Lengend Snippet: Effect of ANP on mRNA expression levels of IL-1β, TNF-α, CCL2, and CCR2 in the aorta. (A) mRNA expression levels of IL-1β, (B) mRNA expression levels of TNF-α, (C) mRNA expression levels of CCL2, (D) mRNA expression levels of CCR2. Compared with control group, # p

    Article Snippet: Reagents Main reagents used in the study were as follows: 1) ANP (Guangzhou Baiyunshan Zhongyi Pharmaceutical Co, Ltd, Lot: WA0076); 2) Simvastatin (Shangdong Xinqi Pharmaceutical Co., Ltd, Lot: 20170101); 3) High fat feed composed of 3% cholesterol, 0.5% sodium cholate, 0.2% propylthiouracil, 5% sugar, 10% lard, and 81.3% basic feed (Medical Science Experimental Animal Center, Guangdong, China, Lot: 201814); 4) Kits for IL-6, IL-10 (Wuhan Huamei Biological Co, Ltd, Lot: U23013173, U24018179), kit for reverse transcription, fluorescent dyes of SYBR (TAKARA, Lot: AI12361A, AK9304), kit for Masson staining (Sinopharm Chemical Reagent Co, Ltd, Lot: G1006), kit for BCA (Shanghai Beyotime biotechnology, Lot: 051018180514), and kit for ECL plus (Applygen, Lot: P1010); 5) Anti-αSMA, anti-CD11c, anti-CD68, fluorescent secondary antibody with FITC marker, and fluorescent secondary antibody with CY3 marker (Servicebio, Lot: GB130441, GB11058, GB11067, GB223011, GB21303); 6) β-actin, anti-MCP-1 (CST, Lot: 15,2), anti-CCR2, anti-Foxp3, anti-IL-1β, anti-TNF-α (Abcam, Lot: GR286626-10, GR239541-14, GR309542-2, GR235155-19), anti-RORγ (Santa, Lot: F3017), anti-MMP-2, and anti-MMP-9 (Wanleibio, Lot: WL03334, WL02141); 7) Horseradish peroxidase-conjugated goat anti-rabbit secondary antibody, horseradish peroxidase-conjugated goat anti-mouse secondary antibody (Shanghai Beyotime biotechnology, Lot: 040818180510, 040818184521); 8) PE anti-mouse CD25, APC anti-mouse CD127, PE/Cy7 anti-mouse CD4, Alexa Fluor® 488 anti-mouse IL-17A, APC Rat IgG2a κ Isotype Ctrl, PE Rat IgG2b κ Isotype Ctrl, Alexa Fluor® 488 Rat IgG1 κ Isotype Ctrl, PE/Cy7 Rat IgG2a κ Isotype Ctrl, Cell Activation Cocktail with Brefeldin A, 10×RBC Lysis Buffer, Fixation Buffer, 10×Intracellular Staining Permeabilization Wash Buffer (Biolegad, Lot: B247733, B232775, B249463, B259048, B238057, B255375, B236504, B236195, B248910, B250015, B252968, B252856).

    Techniques: Aqueous Normal-phase Chromatography, Expressing

    Effect of ANP on protein expression of IL-1β, TNF-α, CCL2 and CCR2 in the aorta. (A) Western blotting analysis of IL-1β, TNF-α, CCL2, and CCR2. (B) Semi-quantitative analysis of IL-1β protein. The original blot images of IL-1β, TNF-α were shown in Supplementary Figure S4(b) and Figure S4(c) . (C) Semi-quantitative analysis of TNF-α protein, (D) Semi-quantitative analysis of CCL2 protein, (E) Semi-quantitative analysis of CCR2 protein. Compared with control group, ## p

    Journal: Frontiers in Pharmacology

    Article Title: Anti-Atherosclerosis Effect of Angong Niuhuang Pill via Regulating Th17/Treg Immune Balance and Inhibiting Chronic Inflammatory on ApoE-/- Mice Model of Early and Mid-Term Atherosclerosis

    doi: 10.3389/fphar.2019.01584

    Figure Lengend Snippet: Effect of ANP on protein expression of IL-1β, TNF-α, CCL2 and CCR2 in the aorta. (A) Western blotting analysis of IL-1β, TNF-α, CCL2, and CCR2. (B) Semi-quantitative analysis of IL-1β protein. The original blot images of IL-1β, TNF-α were shown in Supplementary Figure S4(b) and Figure S4(c) . (C) Semi-quantitative analysis of TNF-α protein, (D) Semi-quantitative analysis of CCL2 protein, (E) Semi-quantitative analysis of CCR2 protein. Compared with control group, ## p

    Article Snippet: Reagents Main reagents used in the study were as follows: 1) ANP (Guangzhou Baiyunshan Zhongyi Pharmaceutical Co, Ltd, Lot: WA0076); 2) Simvastatin (Shangdong Xinqi Pharmaceutical Co., Ltd, Lot: 20170101); 3) High fat feed composed of 3% cholesterol, 0.5% sodium cholate, 0.2% propylthiouracil, 5% sugar, 10% lard, and 81.3% basic feed (Medical Science Experimental Animal Center, Guangdong, China, Lot: 201814); 4) Kits for IL-6, IL-10 (Wuhan Huamei Biological Co, Ltd, Lot: U23013173, U24018179), kit for reverse transcription, fluorescent dyes of SYBR (TAKARA, Lot: AI12361A, AK9304), kit for Masson staining (Sinopharm Chemical Reagent Co, Ltd, Lot: G1006), kit for BCA (Shanghai Beyotime biotechnology, Lot: 051018180514), and kit for ECL plus (Applygen, Lot: P1010); 5) Anti-αSMA, anti-CD11c, anti-CD68, fluorescent secondary antibody with FITC marker, and fluorescent secondary antibody with CY3 marker (Servicebio, Lot: GB130441, GB11058, GB11067, GB223011, GB21303); 6) β-actin, anti-MCP-1 (CST, Lot: 15,2), anti-CCR2, anti-Foxp3, anti-IL-1β, anti-TNF-α (Abcam, Lot: GR286626-10, GR239541-14, GR309542-2, GR235155-19), anti-RORγ (Santa, Lot: F3017), anti-MMP-2, and anti-MMP-9 (Wanleibio, Lot: WL03334, WL02141); 7) Horseradish peroxidase-conjugated goat anti-rabbit secondary antibody, horseradish peroxidase-conjugated goat anti-mouse secondary antibody (Shanghai Beyotime biotechnology, Lot: 040818180510, 040818184521); 8) PE anti-mouse CD25, APC anti-mouse CD127, PE/Cy7 anti-mouse CD4, Alexa Fluor® 488 anti-mouse IL-17A, APC Rat IgG2a κ Isotype Ctrl, PE Rat IgG2b κ Isotype Ctrl, Alexa Fluor® 488 Rat IgG1 κ Isotype Ctrl, PE/Cy7 Rat IgG2a κ Isotype Ctrl, Cell Activation Cocktail with Brefeldin A, 10×RBC Lysis Buffer, Fixation Buffer, 10×Intracellular Staining Permeabilization Wash Buffer (Biolegad, Lot: B247733, B232775, B249463, B259048, B238057, B255375, B236504, B236195, B248910, B250015, B252968, B252856).

    Techniques: Aqueous Normal-phase Chromatography, Expressing, Western Blot

    TLR4, MCP-1, IgA, and caspase-3 expression in rat kidney tissues. ( a ) TLR4, IgA, MCP-1, and caspase-3 expression levels were analyzed by Western blotting. ( b ) Quantitative analysis of TLR4, IgA, MCP-1, and caspase-3 protein levels. A: Healthy, normal controls; B: IgAN model group; C: prednisone acetate group; D: tripterygium glycoside tablet group; E–G: treatment group that received 0.5, 1, and 2 g/kg periostracum cicadae. Data represent the mean ± standard deviation (** p

    Journal: International Journal of Molecular Sciences

    Article Title: Effects of Periostracum Cicadae on Cytokines and Apoptosis Regulatory Proteins in an IgA Nephropathy Rat Model

    doi: 10.3390/ijms19061599

    Figure Lengend Snippet: TLR4, MCP-1, IgA, and caspase-3 expression in rat kidney tissues. ( a ) TLR4, IgA, MCP-1, and caspase-3 expression levels were analyzed by Western blotting. ( b ) Quantitative analysis of TLR4, IgA, MCP-1, and caspase-3 protein levels. A: Healthy, normal controls; B: IgAN model group; C: prednisone acetate group; D: tripterygium glycoside tablet group; E–G: treatment group that received 0.5, 1, and 2 g/kg periostracum cicadae. Data represent the mean ± standard deviation (** p

    Article Snippet: The proteins were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and transferred onto a polyvinylidene fluoride (PVDF) membrane (Millipore Corp., Billerica, MA, USA), which was then incubated with an anti-TLR4 antibody (Cell Signaling Technology, Lexington, KY, USA), an anti-IgA antibody (Cell Signaling Technology), an anti-caspase 3 antibody (Cell Signaling Technology), an anti-MCP-1 antibody (Cell Signaling Technology), and anti-β-actin antibody (Cell Signaling Technology) at 4 °C overnight.

    Techniques: Expressing, Western Blot, Standard Deviation

    MCP-1 induces intracellular calcium increase in DRG neurons following paclitaxel treatment

    Journal: The journal of pain : official journal of the American Pain Society

    Article Title: Induction of monocyte chemoattractant protein-1 (MCP-1) and its receptor CCR2 in primary sensory neurons contributes to paclitaxel-induced peripheral neuropathy

    doi: 10.1016/j.jpain.2013.03.012

    Figure Lengend Snippet: MCP-1 induces intracellular calcium increase in DRG neurons following paclitaxel treatment

    Article Snippet: The increase in MCP-1 was detected as early as 4 hours after the initiation of the treatment and remained at the peak level through day 7.

    Techniques:

    Intracellular calcium response of DRG neurons to MCP-1. A, B . MCP-1 (1 µg/ml) induced increases in intracellular calcium concentration in large (#1 and 2) and medium-sized (#3) neurons which did not respond to capsaicin (0.5 µM) but did

    Journal: The journal of pain : official journal of the American Pain Society

    Article Title: Induction of monocyte chemoattractant protein-1 (MCP-1) and its receptor CCR2 in primary sensory neurons contributes to paclitaxel-induced peripheral neuropathy

    doi: 10.1016/j.jpain.2013.03.012

    Figure Lengend Snippet: Intracellular calcium response of DRG neurons to MCP-1. A, B . MCP-1 (1 µg/ml) induced increases in intracellular calcium concentration in large (#1 and 2) and medium-sized (#3) neurons which did not respond to capsaicin (0.5 µM) but did

    Article Snippet: The increase in MCP-1 was detected as early as 4 hours after the initiation of the treatment and remained at the peak level through day 7.

    Techniques: Concentration Assay

    The induction of MCP-1 in SDH by Paclitaxel. A . Immunostaining shows marked upregulation of MCP-1 in SDH following paclitaxel treatment. B . The increase of MCP-1 is observed as early as 4 hours and persists through 14 days after treatment. C . Double immunostaining

    Journal: The journal of pain : official journal of the American Pain Society

    Article Title: Induction of monocyte chemoattractant protein-1 (MCP-1) and its receptor CCR2 in primary sensory neurons contributes to paclitaxel-induced peripheral neuropathy

    doi: 10.1016/j.jpain.2013.03.012

    Figure Lengend Snippet: The induction of MCP-1 in SDH by Paclitaxel. A . Immunostaining shows marked upregulation of MCP-1 in SDH following paclitaxel treatment. B . The increase of MCP-1 is observed as early as 4 hours and persists through 14 days after treatment. C . Double immunostaining

    Article Snippet: The increase in MCP-1 was detected as early as 4 hours after the initiation of the treatment and remained at the peak level through day 7.

    Techniques: Immunostaining, Double Immunostaining

    Paclitaxel induces the prominent expression of MCP-1 ( A ) and CCR2 ( B ) in both C7 and T5/6 DRGs. Tissues were examined on day 14 after chemotherapy. * p

    Journal: The journal of pain : official journal of the American Pain Society

    Article Title: Induction of monocyte chemoattractant protein-1 (MCP-1) and its receptor CCR2 in primary sensory neurons contributes to paclitaxel-induced peripheral neuropathy

    doi: 10.1016/j.jpain.2013.03.012

    Figure Lengend Snippet: Paclitaxel induces the prominent expression of MCP-1 ( A ) and CCR2 ( B ) in both C7 and T5/6 DRGs. Tissues were examined on day 14 after chemotherapy. * p

    Article Snippet: The increase in MCP-1 was detected as early as 4 hours after the initiation of the treatment and remained at the peak level through day 7.

    Techniques: Expressing

    Blockade of MCP-1 or CCR2 attenuates paclitaxel-induced mechanical hypersensitivity. A . Intrathecal anti-MCP-1 IgG prevents paclitaxel-induced mechanical hypersensitivity (n = 7, 7, 5 and 6 for non-specific (NS) IgG/vehicle, NS IgG/paclitaxel, anti-MCP-1/vehicle

    Journal: The journal of pain : official journal of the American Pain Society

    Article Title: Induction of monocyte chemoattractant protein-1 (MCP-1) and its receptor CCR2 in primary sensory neurons contributes to paclitaxel-induced peripheral neuropathy

    doi: 10.1016/j.jpain.2013.03.012

    Figure Lengend Snippet: Blockade of MCP-1 or CCR2 attenuates paclitaxel-induced mechanical hypersensitivity. A . Intrathecal anti-MCP-1 IgG prevents paclitaxel-induced mechanical hypersensitivity (n = 7, 7, 5 and 6 for non-specific (NS) IgG/vehicle, NS IgG/paclitaxel, anti-MCP-1/vehicle

    Article Snippet: The increase in MCP-1 was detected as early as 4 hours after the initiation of the treatment and remained at the peak level through day 7.

    Techniques:

    The induction of MCP-1 in DRG by Paclitaxel. A . Immunostaining shows marked upregulation of MCP-1 in DRG neurons from paclitaxel-treated animals compared to vehicletreated or naïve animals. B . The increase of MCP-1 is observed as early as 4 hours

    Journal: The journal of pain : official journal of the American Pain Society

    Article Title: Induction of monocyte chemoattractant protein-1 (MCP-1) and its receptor CCR2 in primary sensory neurons contributes to paclitaxel-induced peripheral neuropathy

    doi: 10.1016/j.jpain.2013.03.012

    Figure Lengend Snippet: The induction of MCP-1 in DRG by Paclitaxel. A . Immunostaining shows marked upregulation of MCP-1 in DRG neurons from paclitaxel-treated animals compared to vehicletreated or naïve animals. B . The increase of MCP-1 is observed as early as 4 hours

    Article Snippet: The increase in MCP-1 was detected as early as 4 hours after the initiation of the treatment and remained at the peak level through day 7.

    Techniques: Immunostaining