Angiotensin II enhances the increase in monocyte chemoattractant protein-1 production induced by tumor necrosis factor-α from 3T3-L1 preadipocytes
Monocyte
3T3-L1
DOI:
10.1677/joe-08-0363
Publication Date:
2009-05-09T00:39:04Z
AUTHORS (17)
ABSTRACT
Monocyte chemoattractant protein-1 (MCP-1) and angiotensin II (Ang II) in adipose tissue are thought to induce systemic insulin resistance rodents; but the precise mechanism is not fully clarified. We examined of Ang II-induced and/or tumor necrosis factor-α (TNF-α)-induced MCP-1 production from 3T3-L1 preadipocytes. The protein mRNA expression preadipocytes were increased significantly by stimulation with TNF-α. found no significant increase concentrations alone; it enhanced TNF-α-induced a dose-dependent manner. Then, we effect TNF-α on phosphorylation extracellular signal-regulated kinase (ERK), p38MAPK, IκB-α. clearly ERK p38MAPK phosphorylation. IκB-α was TNF-α, II. induced co-stimulation inhibited either inhibitor, inhibitor or NF-κB inhibitor. Moreover, activation AP-1 (c-fos) Our results suggest that may serve as an additional stimulus through ERK-and p38MAPK-dependent pathways probably due activation.
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