共 21 条
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.
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页码:226 / 235
页数:10
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