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Cellular and Molecular Biology Letters

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Volume 16, Issue 2 (Jun 2011)

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

Yanping Fu / Gang Shi / Yong Wu / Yasuyuki Kawai / Qing Tian / Linlin Yue / Qinjie Xia / Isamu Miyamori / Chunyuan Fan
Published Online: 2011-03-26 | DOI: https://doi.org/10.2478/s11658-011-0002-3

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.

Keywords: Aldosterone; Mitochondria; ATF-1; NOX1; VSMC

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About the article

Published Online: 2011-03-26

Published in Print: 2011-06-01


Citation Information: Cellular and Molecular Biology Letters, ISSN (Online) 1689-1392, DOI: https://doi.org/10.2478/s11658-011-0002-3.

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© 2011 Versita Warsaw. This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License. BY-NC-ND 3.0

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