IR@PKUHSC  > 北京大学基础医学院  > 医学信息学系
学科主题医学信息学
Insulin decreases myocardial adiponectin receptor 1 expression via PI3K/Akt and FoxO1 pathway
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
2012
DOI10.1093/cvr/cvr273
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
WOS记录号WOS:000298381600012
项目编号30871014 ; 2007CB512004
资助机构National Nature Science Foundation of China ; National Basic Research Program of China (973 Program)
引用统计
被引频次:30[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/65968
专题北京大学基础医学院_医学信息学系
北京大学基础医学院
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
推荐引用方式
GB/T 7714
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.
APA Cui, Xiao-Bing.,Wang, Cheng.,Li, Li.,Fan, Dong.,Zhou, Yun.,...&Wu, Li-Ling.(2012).Insulin decreases myocardial adiponectin receptor 1 expression via PI3K/Akt and FoxO1 pathway.CARDIOVASCULAR RESEARCH,93(1),69-78.
MLA Cui, Xiao-Bing,et al."Insulin decreases myocardial adiponectin receptor 1 expression via PI3K/Akt and FoxO1 pathway".CARDIOVASCULAR RESEARCH 93.1(2012):69-78.
条目包含的文件
文件名称/大小 文献类型 版本类型 开放类型 使用许可
69.full.pdf(646KB)期刊论文作者接受稿开放获取CC BY-NC-SA浏览 请求全文
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Cui, Xiao-Bing]的文章
[Wang, Cheng]的文章
[Li, Li]的文章
百度学术
百度学术中相似的文章
[Cui, Xiao-Bing]的文章
[Wang, Cheng]的文章
[Li, Li]的文章
必应学术
必应学术中相似的文章
[Cui, Xiao-Bing]的文章
[Wang, Cheng]的文章
[Li, Li]的文章
相关权益政策
暂无数据
收藏/分享
文件名: 69.full.pdf
格式: Adobe PDF
此文件暂不支持浏览
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。