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Protein Kinase C-δ Is Involved in Induction of NOX1 Gene Expression by Aldosterone in Rat Vascular Smooth Muscle Cells

Haiyan Wei1#, Xuhua Mi2#, Ling Ji2, Lichuan Yang2, Qingjie Xia2, Yuquan Wei3, Isamu Miyamori4, and ChunYuan Fan2*

1State Key Laboratory of Biotherapy, West China Hospital and School of Life Science, Sichuan University, Chengdu, China

2Department of Nephrology, State Key Laboratory of Biotherapy, West China Hospital, West China Medical School, Sichuan University, 1# Keyuan Road 4, Gaopeng Street, High Technological Development Zone, Chengdu 610041, China; fax: 86(28)8516-4005; E-mail: fanchunyuan2009@yahoo.cn; fanchunyuan38@yahoo.com.cn

3State Key Laboratory of Biotherapy, West China Hospital, Chengdu, China

4Third Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, Japan

# These authors contributed equally to this work.

* To whom correspondence should be addressed.

Received June 1, 2009; Revision received August 7, 2009
In this study, we focused on the relationship between aldosterone and NOX1 expression in vascular smooth muscle cells (VSMCs). For the first time, with the use of specific inhibitors of protein kinase C (PKC), we report that PKCδ mediates upregulation of NOX1 induced by 10 nM aldosterone in cultured VSMCs. Participation of PKC in the mediation of NOX1 regulation was further confirmed by the effect of diacylglycerol, a PKC agonist, on the NOX1 RNA in A7r5 cells with Northern blot analysis. To establish cause and effect, we next silenced the PKCδ gene partly by RNA interference and found knockdown of PKCδ gene attenuated aldosterone-induced NOX1 expression, generation of superoxide, as well as protein synthesis in VSMCs. Taken together, these data indicated PKCδ might mediate aldosterone-dependent NOX1 upregulation in VSMCs. In addition, we showed that the cascade from aldosterone to PKCδ activation had the participation of the mineralocorticoid receptor.
KEY WORDS: aldosterone, NOX1, PKCδ

DOI: 10.1134/S0006297910030065