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PMID |
Sentence |
1 |
21866094
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PDGF-A, -B, and both PDGF receptor chain mRNAs, fibronectin, type IV collagen, RANTES, MCP-1, and CCR-2 mRNAs were all increased in the renal cortex of PDGF-D transgenic mice.
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2 |
16263740
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PD98059, an inhibitor of ERK, partially prevented CML-induced MCP-1 gene expression.
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3 |
16263740
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Parthenolide and mithramycin A, inhibitors of NF-kappaB and Sp1, respectively, abolished CML-induced MCP-1 gene expression in a dose-dependent manner.
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4 |
16263740
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NF-kappaB and Sp1 regulate MCP-1 gene transcription.
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5 |
17604001
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We found that, in glomerular podocytes, induction of monocyte chemoattractant protein 1 (MCP-1) and inducible nitric oxide synthase (iNOS) by TNF-alpha was abrogated by K-7174.
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6 |
17604001
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Furthermore, K-7174-elicited UPR abrogated induction of MCP-1 and iNOS not only by TNF-alpha but also by medium conditioned by activated macrophages.
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7 |
19420107
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Glomerular podocytes in culture, verified to express the marker nephrin, were exposed to diabetic mediators such as high glucose or angiotensin II and assayed for MCP-1.
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8 |
19420107
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The TGF-beta-induced MCP-1 was found to activate the podocyte's cysteine-cysteine chemokine receptor 2 (CCR2) and, as a result, enhance the cellular motility, cause rearrangement of the actin cytoskeleton, and increase podocyte permeability to albumin in a Transwell assay.
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9 |
19420107
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The preceding effects of TGF-beta were replicated by treatment with recombinant MCP-1 and blocked by a neutralizing anti-MCP-1 antibody or a specific CCR2 inhibitor, RS102895.
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10 |
19420107
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In conclusion, this is the first description that TGF-beta signaling through PI3K induces the podocyte expression of MCP-1 that can then operate via CCR2 to increase cellular migration and alter albumin permeability characteristics.
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11 |
20375985
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Furthermore, visfatin induced tyrosine phosphorylation of the insulin receptor, activated downstream insulin signaling pathways such as Erk-1, Akt, and p38 MAPK, and markedly increased the levels of TGFbeta1, PAI-1, type I collagen, and MCP-1 in both renal cells.
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12 |
20953353
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TWEAK promotes the secretion of MCP-1 and RANTES through NF-kappaB RelA-containing complexes and upregulates CCl21 and CCL19 expression through NF-kappaB inducing kinase (NIK-) dependent RelB/NF-kappaB2 complexes.
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13 |
20660016
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Because TRB3 inhibits MCP-1, manipulation of TRB3 expression could provide a novel therapeutic approach in diabetic kidney disease.
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14 |
18799549
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We found that, in murine podocytes, expression of monocyte chemoattractant protein 1 (MCP-1) in response to TNF-alpha was suppressed by indomethacin but not by ibuprofen.
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15 |
18799549
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In tumor necrosis factor (TNF)-alpha-treated cells, suppression of MCP-1 by indomethacin was inversely correlated with induction of UPR, and other inducers of UPR including tunicamycin, thapsigargin, and A23187 reproduced the suppressive effect.
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16 |
18799549
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Subsequent experiments revealed that acute ablation of GRP78 protein by AB5 subtilase cytotoxin caused reinforcement of MCP-1 induction and NF-kappaB activation by TNF-alpha and that transfection with GRP78 significantly suppressed the cytokine-induced activation of NF-kappaB.
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17 |
15918915
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Gene expression of ICAM-1, VCAM-1 and RANTES was unaltered whereas Osteopontin and MCP-1 were induced by hypertension.
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18 |
21703397
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CCL2 blockade reduced glomerular leukocyte counts and renal-inducible nitric oxide synthase or IL-6 mRNA expression.
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19 |
19887845
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Knockdown of TLR2 and TLR4 inhibited the fibrinogen-induced MCP-1 mRNA upregulation.
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20 |
16130407
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IP-10 correlated IL-18, IL-6, TNF-alpha and MCP-1.
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21 |
21810593
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In addition, AM1241 reduced CCR2 expression in both renal cortex and cultured podocytes, suggesting that CB2 activation may interfere with the deleterious effects of MCP-1 signaling.
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