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PMID |
Sentence |
1 |
16288986
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Neither IL-1beta nor TNFalpha alone has an effect on nephrin promoter activity suggesting that additional posttranscriptional regulatory events might be operative.
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2 |
16288986
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In the presence of PPARalpha agonists, IL-1beta or TNFalpha, the decay of nephrin mRNA was drastically reduced thus arguing for an additional posttranscriptional mode of action.
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3 |
16205945
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The expression of NF-kappaB subunits p65 and p50, and the NF-kappaB regulated proinflammatory mediators tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1) as well as CD68 and synaptopodin was examined by Southwestern histochemistry (SWH) or immunohistochemistry.
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4 |
16514436
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Furthermore, TNFalpha and IL-18 phosphorylated neutrophil p38 mitogen-activated protein kinase (MAPK), but IL-18-mediated p38 MAPK phosphorylation was unaffected by anti-TNFalpha antibody.
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5 |
16626513
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Increased TNF-alpha in plasma and glomeruli may upregulate Ang2 expression in glomeruli.
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6 |
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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7 |
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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8 |
19240767
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TNF-related apoptosisinducing ligand (TRAIL) and osteoprotegerin had the highest level of expression.
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9 |
20953353
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Tumor necrosis factor (TNF) and Fas ligand regulate renal cell survival and inflammation, and therapeutic targeting improves the outcome of experimental renal injury.
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10 |
20953353
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TNF-related apoptosis-inducing ligand (TRAIL and its potential decoy receptor osteoprotegerin are the two most upregulated death-related genes in human diabetic nephropathy.
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11 |
20953353
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While TNF only activates canonical NF-kappaB signaling, TWEAK promotes both canonical and noncanonical NF-kappaB activation in tubular cells, regulating different inflammatory responses.
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12 |
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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13 |
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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14 |
18799549
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Reporter assays showed that indomethacin as well as thapsigargin attenuated activation of NF-kappaB by TNF-alpha, and it was associated with enhanced degradation of TNF receptor-associated factor 2 (TRAF2) and blunted degradation of IkappaBbeta.
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15 |
20237236
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We previously reported that 1) expression of nephrin in cultured podocytes is reinforced by retinoic acid (RA) and 1,25-dihydroxyvitamin D(3), 2) these effects are mediated by retinoic acid receptor (RAR) and vitamin D receptor (VDR), and 3) basal and inducible expression of nephrin is downregulated by TNF-alpha.
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16 |
20237236
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In the present investigation, we identified that TNF-alpha selectively represses activity of RAR but not VDR.
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17 |
20237236
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To elucidate mechanisms underlying this observation, we tested involvement of downstream targets for TNF-alpha: nuclear factor-kappaB (NF-kappaB), mitogen-activated protein (MAP) kinases, phosphatidylinositol 3-kinase (PI3K)-Akt, and cAMP-protein kinase A (PKA).
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18 |
20237236
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TNF-alpha caused activation of NF-kappaB, MAP kinases, and PI3K-Akt in podocytes, whereas blockade of these molecules did not affect inhibition of RAR by TNF-alpha.
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19 |
16130407
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IP-10 correlated IL-18, IL-6, TNF-alpha and MCP-1.
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