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学科主题: 医学信息学
题名:
Insulin decreases myocardial adiponectin receptor 1 expression via PI3K/Akt and FoxO1 pathway
作者: Cui, Xiao-Bing1,2; Wang, Cheng1,2; Li, Li1,2; Fan, Dong1,2; Zhou, Yun1,2; Wu, Dan1,2; Cui, Qing-Hua3; Fu, Feng-Ying1,2; Wu, Li-Ling1,2,4
关键词: Adiponectin receptor ; Cardiomyocyte ; Insulin ; FoxO1
刊名: CARDIOVASCULAR RESEARCH
发表日期: 2012
DOI: 10.1093/cvr/cvr273
卷: 93, 期:1, 页:69-78
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cardiac & Cardiovascular Systems
研究领域[WOS]: Cardiovascular System & Cardiology
关键词[WOS]: ISCHEMIA-REPERFUSION INJURY ; GENE-EXPRESSION ; DIABETIC MICE ; RESISTANCE ; HEART ; HYPERINSULINEMIA ; ASSOCIATION ; HYPOADIPONECTINEMIA ; SENSITIVITY ; DISRUPTION
英文摘要:

Aims Adiponectin is considered an important adipokine protecting against diabetes, atherosclerosis, and cardiovascular disease. Because adiponectin receptors (AdipoRs) are critical components in the adiponectin signalling cascade, we investigated the effect of insulin on the expression of myocardial AdipoRs and explored the possible molecular mechanism.

Methods and results The hyperinsulinaemia rat model was induced by infusion of insulin (1 U/day) for 28 days: serum and myocardial adiponectin levels were increased, and skeletal muscle and myocardial AdipoR1 expression and AMP-activated protein kinase (AMPK) phosphorylation were decreased. In primary cultured neonatal rat ventricular myocytes (NRVMs), insulin decreased AdipoR1 but not AdipoR2 expression and AMPK phosphorylation; high glucose had no affect on AdipoRs expression. Akt and extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation was increased in insulin-treated hearts and in NRVMs. P13K inhibitor LY294002 and Akt1/2 kinase inhibitor but not the ERK1/2 kinase (MEK) inhibitors PD98059 and U0126 blocked the insulin-induced reduction in AdipoR1 expression and AMPK phosphorylation. Insulin induced forkhead/winged helix box gene group O-1 (FoxO1) phosphorylation and translocation from the nucleus to the cytosol, and this was blocked by LY294002. FoxO1 small interfering RNA reduced AdipoR1 expression and AMPK phosphorylation. In electrophoretic mobility shift assay and chromatin immunoprecipitation, FoxO1 bound to the putative site from -167 to -157 bp of the AdipoR1 promoter both in vitro and in living cells; insulin suppressed this binding, which was blocked by LY294002.

Conclusion Insulin inhibits myocardial AdipoR1 expression via PI3K/Akt and FoxO1 pathways, and FoxO1 mediates AdipoR1 transcription by binding to its promoter directly.

语种: 英语
所属项目编号: 30871014 ; 2007CB512004
项目资助者: National Nature Science Foundation of China ; National Basic Research Program of China (973 Program)
WOS记录号: WOS:000298381600012
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/65968
Appears in Collections:基础医学院_医学信息学系_期刊论文

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作者单位: 1.Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Dept Biomed Informat, Beijing 100191, Peoples R China
3.Peking Univ, Minist Hlth, Key Lab Cardiovasc Mol Biol & Regulatory Peptides, Beijing 100191, Peoples R China
4.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100191, Peoples R China

Recommended Citation:
Cui, Xiao-Bing,Wang, Cheng,Li, Li,et al. Insulin decreases myocardial adiponectin receptor 1 expression via PI3K/Akt and FoxO1 pathway[J]. CARDIOVASCULAR RESEARCH,2012,93(1):69-78.
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