Interleukin-1β-induced Cyclooxygenase-2 Expression Requires Activation of Both c-Jun NH2-terminal Kinase and p38 MAPK Signal Pathways in Rat Renal Mesangial Cells

Guan, Zhonghong; Buckman, Sha Avhree Y.; Miller, Brent W.; Springer, Lisa D.; Morrison, Adam

doi:10.1074/jbc.273.44.28670

Cited by 226 publications

(161 citation statements)

References 27 publications

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“…The p38 MAPK kinase pathway, 49 the JNK pathway 50 and the NF-kB pathway 51 have all been implicated in the upregulation of COX-2 by IL-1b and TNFa. Most of the drugs that inhibit these kinases were products of the search for potent antiinflammatory agents that block the upregulation of COX-2 and thus block PGE 2 formation.…”

Section: Discussionmentioning

confidence: 99%

Regulation of monocyte chemoattractant protein 1 (MCP-1) release by explants of human visceral adipose tissue

Fain

Madan

2005

Int J Obes

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BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1) is a chemokine involved in monocyte recruitment during inflammation whose plasma level is elevated in obesity. OBJECTIVE: The present studies were designed to examine the release of MCP-1 in primary culture by explants of visceral adipose tissue from morbidly obese women. RESULTS: Most of the MCP-1 released by adipose tissue explants was derived from the nonfat cells in adipose tissue. The release of MCP-1 by adipose tissue explants was upregulated almost five-fold between 3 and 48 h of incubation. Approximately half of this upregulation was due to the release of endogenous tumor necrosis factor a (TNFa) and IL-1b based on the ability of a combination of a soluble TNFa receptor (etanercept) and a blocking antibody against IL-1b to reduce MCP-1 release. The release of MCP-1 over 48 h was unaffected by insulin or dexamethasone but significantly reduced by the combination of both agents. MCP-1 release was reduced by 60% in the presence of an inhibitor of the nuclear factor kB (NF-kB) pathway. There were no significant effects of inhibitors of p44/42 mitogen-activated protein kinase (ERK), Jun N-terminal kinase (JNK) and p38 mitogenactivated protein kinase (p38 MAPK) pathways on MCP-1 release. However, inhibition of MCP-1 release in the presence of inhibitors of both the p38 MAPK and NF-kB pathways was greater than that seen with only the NF-kB inhibitor. DISCUSSION: The present data shows that MCP-1 formation is upregulated over a 48-h incubation of primary explants of visceral adipose tissue. Half of this upregulation is dependent upon endogenous TNFa and Il-1b and involves the p38 MAPK and NF-kB pathways.

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Section: Discussionmentioning

confidence: 99%

Regulation of monocyte chemoattractant protein 1 (MCP-1) release by explants of human visceral adipose tissue

Fain

Madan

2005

Int J Obes

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“…Cell signalling through the p38 mitogen-activated protein kinase (MAPK) pathway, involving dual phosphorylation of the Tyr-X-Thr motif of p38 MAPK [4], is known to play a role in both of these processes [5,6,7,8]. Specific inhibition of p38 MAPK signalling is effective in the treatment of human endotoxaemia, and in rat models of inflammatory renal disease, lung fibrosis and arthritis [9,10,11,12,13].…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, advanced glycation, glycoxidation and lipoxidation end-products can stimulate IL-1 and TNF-α production by macrophages [19,20]. IL-1 and TNF-α are potent inducers of p38 MAPK in renal parenchymal cells [6,21] and TGF-β1 stimulates p38 MAPK phosphorylation in mesangial cells and fibroblasts [7,8]. Thus the diabetic milieu could potentially promote p38 MAPK phosphorylation in renal cells by direct and indirect pathways.…”

Section: Introductionmentioning

confidence: 99%

Abnormal p38 mitogen-activated protein kinase signalling in human and experimental diabetic nephropathy

et al. 2004

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Aims/hypothesis. Inflammation and fibrosis are pathological mechanisms that are partially regulated by cell signalling through the p38 mitogen-activated protein kinase (MAPK) pathway. Elements of the diabetic milieu such as high glucose and advanced glycation endproducts induce activation of this pathway in renal cells. Therefore, we examined whether p38 MAPK signalling is associated with the development of human and experimental diabetic nephropathy. Methods. Immunostaining identified phosphorylated (active) p38 MAPK in human biopsies with no abnormality (n=6) and with Type 2 diabetic nephropathy (n=12). Changes in kidney levels of phosphorylated p38 were assessed by immunostaining and western blotting in mice with streptozotocin-induced Type 1 diabetes that had been killed after 0.5, 2, 3, 4 and 8 months, and in Type 2 diabetic db/db mice at 2, 4, 6 and 8 months of age. Results. Phosphorylated p38 was detected in some intrinsic cells in normal human kidney, including podocytes, cortical tubules and occasional interstitial cells. Greater numbers of these phosphorylated p38+ cells were observed in diabetic patients, and phosphorylated p38 was identified in accumulating interstitial macrophages and myofibroblasts. A similar pattern of p38 activation was observed in both mouse models of diabetes. In mice, kidney levels of phosphorylated p38 increased (2-6 fold) following the onset of Type 1 and Type 2 diabetes. In both mouse models, interstitial phosphorylated p38+ cells were associated with hyperglycaemia, increased HbA 1 c levels and albuminuria. Further assessment of streptozotocin-induced diabetic nephropathy showed that interstitial phosphorylated p38+ cells correlated with interstitial fibrosis (myofibroblasts, collagen). Conclusions/interpretation. Increased p38 MAPK signalling is a feature of human and experimental diabetic nephropathy. Time course studies in mouse models suggest that phosphorylation of p38 plays a pathological role, particularly in the development of interstitial fibrosis.

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“…MAPK signalling pathway is also involved in the inflammatory process and has been extensively investigated. Recently studies suggested that the MAPK pathways also play a role in regulating PGE 2 expression (Guan et al, 1998;Rodriguez-Barbero et al, 2006). Therefore, we have demonstrated that activation of MAPK pathways induce COX-2 expression and PGE2 synthesis in LPS-stimulated RAW264.7 cells.…”

Section: Discussionmentioning

confidence: 68%

Suppression Effect of the Inflammatory Response in Macrophages by Paeoniae Radix Rubra Extracts

Bak¹,

Son²,

Kim³

et al. 2011

Korean Journal of Medicinal Crop Science

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: Paeoniae Radix Rubra is a preparation consisting of desiccated roots of Paeonia lactiflora PALL (belonging to Ranunculaceae). Paeoniae Radix Rubra is used as a medicinal herb in Asian countries to treat many diseases. Ethanol-or water-based extracts of Paeoniae Radix Rubra were prepared and tested on RAW 264.7 cells, a murine macrophage cell line. The expression of some pro-inflammatory proteins, including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphorylated ERK1/2 was detected by Western blot analyses, while PGE2 expression was quantified by ELISA. Both the water and ethanol extracts of Paeoniae Radix Rubra suppressed LPS-induced nitric oxide (NO) production and exhibited cell toxicity in accordance with increased NO production. Also, both extracts reduced the expression of COX-2 and iNOS, and inhibited phosphorylation of ERK1/2 in LPS-stimulated RAW 264.7 cells. Extracts prepared from Paeoniae Radix Rubra contain anti-inflammatory agents that inhibit the iNOS and MAPK pathways.

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Interleukin-1β-induced Cyclooxygenase-2 Expression Requires Activation of Both c-Jun NH2-terminal Kinase and p38 MAPK Signal Pathways in Rat Renal Mesangial Cells

Cited by 226 publications

References 27 publications

Regulation of monocyte chemoattractant protein 1 (MCP-1) release by explants of human visceral adipose tissue

Regulation of monocyte chemoattractant protein 1 (MCP-1) release by explants of human visceral adipose tissue

Abnormal p38 mitogen-activated protein kinase signalling in human and experimental diabetic nephropathy

Suppression Effect of the Inflammatory Response in Macrophages by Paeoniae Radix Rubra Extracts

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