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

被引:4
作者
Fu, Yanping [1 ]
Shi, Gang [2 ]
Wu, Yong [3 ]
Kawai, Yasuyuki [4 ]
Tian, Qing [1 ]
Yue, Linlin [1 ]
Xia, Qinjie [1 ]
Miyamori, Isamu [4 ]
Fan, Chunyuan [1 ,5 ]
机构
[1] Sichuan Univ, Dept Nephrol, W China Hosp, Chengdu 610041, Peoples R China
[2] Sichuan Univ, State Key Lab Biotherapy, Chengdu 610041, Peoples R China
[3] Second Outpatient Inst Chengdu Mil Reg, Chengdu 610041, Peoples R China
[4] Univ Fukui, Dept Internal Med 3, Fac Med Sci, Fukui 910, Japan
[5] Second Peoples Hosp Chengdu, Chengdu 610041, Peoples R China
关键词
Aldosterone; Mitochondria; ATF-1; NOX1; VSMC; SMOOTH-MUSCLE; NADPH OXIDASE; SPIRONOLACTONE; SURVIVAL;
D O I
10.2478/s11658-011-0002-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 PGF2 alpha 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.
引用
收藏
页码:226 / 235
页数:10
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