Aldosterone-induced inflammatory response of mesangial cells via angiotension II receptors.

Introduction: In this study, we investigated whether AngII receptors (AT1a and AT2) contributed to the development of the aldosterone-induced inflammatory response of rat mesangial cells (RMCs). Materials and methods: RMCs were isolated from the glomeruli of normal or diabetic rats which were produced by injection of streptozotocin, and cultured in high-glucose media. In order to evaluate the effects of aldosterone, the expression of AT1a, AT2, NF-B and MCP-1 was detected. In addition, in order to evaluate the role of Ang II receptors, AT1a and AT2 genes were blocked and the expression of NF-B and MCP-1 was detected. Moreover, for assessing the relationship between NF-B and MCP-1, the NF-B gene was blocked and MCP-1 expression was detected. Results: Aldosterone significantly increased AT1a, AT2, NF-B and MCP-1 levels in RMCs in a dose-dependent manner, whereas eplerenone (EPI), a selective aldosterone antagonist, partly inhibited the effects of aldosterone. When AT1a and AT2 genes were blocked, the expression of NF-B and MCP-1 was greatly inhibited. Moreover, when the NF-B gene was silenced, the expression of MCP-1 was reduced. Conclusion: We demonstrated that aldosterone induced an inflammatory response in RMCs cultured in high-glucose media via the AT1a and AT2 pathways.