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学科主题: 临床医学
题名:
A distinct AMP-activated protein kinase phosphorylation site characterizes cardiac hypertrophy induced by l-thyroxine and angiotensin II
作者: Jiang, Sheng-Yang; Xu, Ming; Ma, Xiao-Wei; Xiao, Han; Zhang, You-Yi1
关键词: AMP-activated protein kinase ; angiotensin II ; cardiac hypertrophy ; l-thyroxine ; phosphorylation
刊名: CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
发表日期: 2010-09-01
DOI: 10.1111/j.1440-1681.2010.05404.x
卷: 37, 期:9, 页:919-925
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Pharmacology & Pharmacy ; Physiology
研究领域[WOS]: Pharmacology & Pharmacy ; Physiology
关键词[WOS]: MYOSIN HEAVY-CHAIN ; PRESSURE-OVERLOAD HYPERTROPHY ; LEFT-VENTRICULAR HYPERTROPHY ; CARDIOMYOCYTE HYPERTROPHY ; SIGNALING PATHWAY ; MESSENGER-RNA ; AKT ACTIVITY ; RAT HEARTS ; EXPRESSION ; ISOPROTERENOL
英文摘要:

P>1. The purpose of the present study was to evaluate differences in the AMP-activated protein kinase (AMPK) phosphorylation sites in cardiac hypertrophy induced by l-thyroxine and angiotensin (Ang) II.

2. Cardiac hypertrophy was induced in wild-type and AMPK alpha 2-knockout mice by treatment with 1 mg/kg, i.p., thyroxine or 1.44 mg/kg per day AngII for 14 days. The phenotype of the hypertrophy was evaluated using echocardiographic measurments and histological analyses. The phosphorylation of AMPK at alpha-Ser485/491 and alpha-Thr172 was determined by western blot analysis.

3. In wild-type mice, the phosphorylation of AMPK alpha-Ser485/491 was significantly elevated in the AngII-treated group, but not in the thyroxine-reated group, compared with the vehicle control group. In contrast, the phosphorylation of AMPK alpha-Thr172 was significantly increased by thyroxine, but not AngII, treatment compared with the vehicle control group. Furthermore, knockout of the AMPK alpha 2 subunit abolished phosphorylation at the alpha-Ser485/491 site and significantly suppressed phosphorylation at the alpha-Thr172 site, resulting in alleviation of thyroxine- but not AngII-induced hypertrophy.

4. In conclusion, l-thyroxine and AngII induce the phosphorylation of distinct sites of AMPK in cardiac hypertrophy. Phosphorylation of AMPK alpha-Thr172 may contribute to thyroxine-induced cardiac hypertrophy.

语种: 英语
所属项目编号: 2006CB503806 ; 30672466 ; 30821001 ; 7082101
项目资助者: National Key Basic Research Program of China ; Natural Science Foundation of China ; Natural Science Foundation of Beijing
WOS记录号: WOS:000281219600010
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/67599
Appears in Collections:北京大学第三临床医学院_心血管内科_期刊论文

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作者单位: 1.Peking Univ, Hosp 3, Inst Vasc Med, Beijing 100191, Peoples R China
2.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing, Peoples R China

Recommended Citation:
Jiang, Sheng-Yang,Xu, Ming,Ma, Xiao-Wei,et al. A distinct AMP-activated protein kinase phosphorylation site characterizes cardiac hypertrophy induced by l-thyroxine and angiotensin II[J]. CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY,2010,37(9):919-925.
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