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Monocyte chemoattractant protein-1 (MCP-1) and angiotensin II (Ang II) in adipose tissue are thought to induce systemic insulin resistance in rodents; but the precise mechanism is not fully clarified. We examined the mechanism of Ang II-induced and/or tumor necrosis factor-a (TNF-a)-induced MCP-1 production from 3T3L1 preadipocytes. The MCP-1 protein and MCP-1 mRNA expression in 3T3-L1 preadipocytes were increased significantly by stimulation with TNF-a. We found no significant increase in MCP-1 concentrations by Ang II alone; but it enhanced the TNF-a-induced MCP-1 mRNA expression in a dose-dependent manner. Then, we examined the effect of Ang II and/or TNF-a on phosphorylation of extracellular Journal of Endocrinology (2009) 202, 199–205 0022–0795/09/0202–199 q 2009 Society for Endocrinology Printed in Great signal-regulated kinase (ERK), p38MAPK, and IkB-a. Ang II and TNF-a clearly enhanced ERK and p38MAPK phosphorylation. IkB-a phosphorylation was enhanced by TNF-a, but not by Ang II. The MCP-1 mRNA expression induced by TNF-a and co-stimulation with Ang II was inhibited by either ERK inhibitor, p38MAPK inhibitor or NF-kB inhibitor. Moreover, Ang II enhanced the activation of AP-1 (c-fos) induced by TNF-a. Our results suggest that Ang II may serve as an additional stimulus on the TNF-a-induced MCP-1 production through the ERKand p38MAPK-dependent pathways probably due to AP-1 activation. Journal of Endocrinology (2009) 202, 199–205

Angiotensin II enhances the increase in monocyte chemoattractant protein-1 production induced by tumor necrosis factor-α from 3T3-L1 preadipocytes