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1 Department of Clinical and Molecular Endocrinology, Tokyo Medical and Dental University Graduate School, Tokyo, Japan; Department of Clinical and Molecular Endocrinology, Tokyo Medical and Dental University Graduate School, Tokyo, Japan
2 Department of Clinical and Molecular Endocrinology, Tokyo Medical and Dental University Graduate School, Tokyo, Japan
* To whom correspondence should be addressed. E-mail: tyoshimoto.cme{at}tmd.ac.jp.
Both monocyte chemoattractant protein-1 (MCP-1), a member of chemokine family, and angiotensinogen, a precursor of angiotensin (Ang) II, are produced by adipose tissue, and increased in obese state. MCP-1 has been shown to decrease insulin-stimulated glucose uptake and several adipogenic genes expression in adipocytes in vitro, suggesting its pathophysiological significance in obesity. However, the pathophysiological interaction between MCP-1 and Ang II in adipose tissue remains unknown. The present study was undertaken to investigate the potential mechanisms by which Ang II affects MCP-1 gene expression in rat primary cultured preadipocytes and adipose tissue in vivo. Ang II significantly increased steady-state MCP-1 mRNA levels in a time- and dose-dependent manner. The Ang II-induced MCP-1 mRNA and protein expression was completely abolished by Ang II type 1 (AT1)-receptor antagonist (valsartan). An antioxidant/NF-
B inhibitor (pyrrolidine dithiocarbamate), and an inhibitor of IB-
phosphorylation (Bay 11-7085) also blocked Ang II-induced MCP-1 mRNA expression.Ang II induced translocation of NF-B p65 subunit from cytoplasm to nucleus by immunocytochemical study. Luciferase assay using reporter constructs containing MCP-1 promoter region revealed that two NF-B binding sites in its enhancer region were essential for the Ang II-induced promoter activities. Furthermore, basal mRNA and protein of MCP-1 during preadipocytes differentiation were significantly greater in preadipocytes than in differentiated adipocytes, whose effect was more pronounced in the presence of Ang II. Exogenous administration of Ang II to rats led to increased MCP-1 expression in epididymal, subcutaneous and mesenteric adipose tissue. In conclusion, our present study demonstrates that Ang II increases MCP-1 gene expression via AT1-receptor-mediated and NF-B-dependent pathway in rat preadipocytes, as well as adipose MCP-1 expression in vivo. Thus, the augmented MCP-1 expression by Ang II in preadipocytes may provide a new link between obesity and cardiovascular disease.
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