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学科主题: 临床医学
题名:
Inhibitory crosstalk between ERK and AMPK in the growth and proliferation of cardiac fibroblasts
作者: Du, Jianhai1; Guan, Tongju1; Zhang, Hui1; Xia, Yi1; Liu, Fei1; Zhang, Youyi1
关键词: AMPK ; ERK ; cardiac fibroblasts
刊名: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
发表日期: 2008-04-04
DOI: 10.1016/j.bbrc.2008.01.099
卷: 368, 期:2, 页:402-407
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology ; Biophysics
研究领域[WOS]: Biochemistry & Molecular Biology ; Biophysics
关键词[WOS]: ACTIVATED-PROTEIN-KINASE ; FACTOR RECEPTOR ; PATHWAY ; TRANSACTIVATION ; INSULIN ; GLUCOSE ; P70S6K ; CELLS ; HEART ; DNA
英文摘要:

Extracellular signal-regulated kinase (ERK) is one of the key protein kinases that regulate the growth and proliferation in cardiac fibroblasts (CFs). As an energy sensor of cellular metabolism, AMP-activated protein kinase (AMPK) is found recently to be involved in myocardial remodeling. In this study, we investigated the crosstalk between ERK and AMPK in the growth and proliferation of CFs. In neonatal rat cardiac fibroblasts (NRCFs), we found that serum significantly inhibited basal AMPK phosphorylation between 10 min and 24 h and also partially inhibited AMPK phosphorylation by AMPK activator, 5-aminoimidazole-4-carboxamide-ribonucleoside (AICAR). Furthermore, ERK inhibitor could greatly reverse the inhibition of AMPK by serum. Conversely, activation of AMPK by AICAR also showed a significant inhibition of basal and serum-induced ERK phosphorylation but it showed a delayed and steadfast inhibition which appeared after 60 min and lasted until 12 h. Moreover, inhibition of ERK could repress the activation of p70S6K, an important kinase in cardiac proliferation, and AICAR could also inhibit p70S6K phosphorylation. In addition, under both serum and serum-free medium, AICAR significantly inhibited the DNA synthesis and cell numbers, and reduced cells at S phase. In conclusion, AMPK activation with AICAR inhibited growth and proliferation in cardiac fibroblasts, which involved inhibitory interactions between ERK and AMPK. This is the first report that AMPK could be a target of ERK in growth factors-induced proliferation, which may give a new mechanism that growth factors utilize in their promotion of proliferation in cardiac fibroblasts. (c) 2008 Elsevier Inc. All rights reserved.

语种: 英语
WOS记录号: WOS:000253669500037
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/51810
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.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100083, Peoples R China
2.Peking Univ, Inst Vasc Med, Hosp 3, Beijing 100083, Peoples R China

Recommended Citation:
Du, Jianhai,Guan, Tongju,Zhang, Hui,et al. Inhibitory crosstalk between ERK and AMPK in the growth and proliferation of cardiac fibroblasts[J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,2008,368(2):402-407.
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