Open Access

The mitochondria mediate the induction of NOX1 gene expression by aldosterone in an ATF-1-dependent manner

  • Yanping Fu1,
  • Gang Shi2,
  • Yong Wu3,
  • Yasuyuki Kawai4,
  • Qing Tian1,
  • Linlin Yue1,
  • Qinjie Xia1,
  • Isamu Miyamori4 and
  • Chunyuan Fan1, 5Email author
Cellular & Molecular Biology LettersAn International Journal201116:2

https://doi.org/10.2478/s11658-011-0002-3

Received: 17 July 2010

Accepted: 3 February 2011

Published: 12 February 2011

Abstract

High aldosterone (Ald) levels can induce hypertrophy of vascular smooth muscle cells (VSMCs), which carries high risks of heart failure. A previous study showed that Ald induces hypertrophy of VSMCs by up-regulating NOX1, a catalytic subunit of NADPH oxidase that produces superoxides. However, the precise mechanism remains unknown. Diphenylene iodonium (DPI) is known as an inhibitor of complex I in the mitochondrial respiratory chain, and it was also found to almost completely suppress the induction of NOX1 mRNA and the phosphorylation of activating transcription factor (ATF-1) by PGF2α or PDGF in a rat VSMC cell line. In this study, we found that the Ald-induced phosphorylation of ATF-1 and NOX1 expression was significantly suppressed by DPI. Silencing of ATF-1 gene expression attenuated the induction of NOX1 mRNA expression, and over-expression of ATF-1 restored Ald-induced NOX1 expression. On the basis of this data, we show that the mitochondria mediate aldosterone-induced NOX1 gene expression in an ATF-1-dependent manner.

Key words

Aldosterone Mitochondria ATF-1 NOX1 VSMC

Notes

Advertisement