SIRT1 inhibits angiotensin Ⅱ-induced vascular smooth muscle cell hypertrophy

Angiotensin Ⅱ （Ang Ⅱ） stimulates vascular smooth muscle cell （VSMC） hypertrophy as a critical event in the development of vascular diseases such as atherosclerosis. Sirtuin （SIRT） 1, a nicotinamide adenine dinucleotide dependent deacetylase, has been demonstrated to exert protective effects in ather...

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Bibliographic Details
Published in:Acta biochimica et biophysica Sinica 2011-02, Vol.43 (2), p.103-109
Main Authors: Li, Li, Gao, Peng, Zhang, Huina, Chen, Houzao, Zheng, Wei, Lv, Xiang, Xu, Tingting, Wei, Yusheng, Liu, Depei, Liang, Chihchuan
Format: Article
Language:English
Subjects:
Angiotensin II
Animals
Cell Line
GATA6 Transcription Factor - genetics
GATA6 Transcription Factor - metabolism
Humans
Hypertrophy - chemically induced
Hypertrophy - genetics
Hypertrophy - metabolism
Hypertrophy - pathology
Mice
Muscle, Smooth, Vascular - metabolism
Muscle, Smooth, Vascular - pathology
NADH, NADPH Oxidoreductases - genetics
NADH, NADPH Oxidoreductases - metabolism
NADPH Oxidase 1
Rats
Sirtuin 1 - genetics
Sirtuin 1 - metabolism
VSMC
动脉粥样硬化
烟酰胺腺嘌呤二核苷酸
细胞肥大
腺病毒介导
血管平滑肌细胞
血管疾病
血管紧张素
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Summary:Angiotensin Ⅱ （Ang Ⅱ） stimulates vascular smooth muscle cell （VSMC） hypertrophy as a critical event in the development of vascular diseases such as atherosclerosis. Sirtuin （SIRT） 1, a nicotinamide adenine dinucleotide dependent deacetylase, has been demonstrated to exert protective effects in atherosclerosis by promoting endothelium-dependent vascular relaxation and reducing macrophage foam cell formation, but its role in VSMC hypertrophy remains unknown. In this study, we tried to investigate the effect of SIRT1 on Ang Ⅱ-induced VSMC hypertrophy. Results showed that adenoviral-mediated over-expression of SIRT1 significantly inhibited Ang Ⅱ- induced VSMC hypertrophy, while knockdown of SIRT1 by RNAi resulted in an increased [^3H]-leucine incorporation of VSMC. Accordingly, nicotinamide adenine dinucleotide phosphate oxidase 1 （Noxl） expression induced by Ang Ⅱ was inhibited by SIRT1 in VSMCs. SIRT1 activator resveratrol decreased, whereas endogenous SIRT1 inhibitor nicotinamide increased Noxl expression in A7r5 VSMCs. Furthermore, transcription factor GATA-6 was involved in the down-regulation of Noxl expression by SIRT1. These results provide new insight into SIRTI＇s anti-atherogenic properties by suppressing Ang Ⅱ-induced VSMC hypertrophy.
ISSN:1672-9145
1745-7270
DOI:10.1093/abbs/gmq104