北京大学医学部机构知识库
Advanced  
IR@PKUHSC  > 北京大学第三临床医学院  > 心血管内科  > 期刊论文
学科主题: 临床医学
题名:
beta(2)-adrenergic receptor-induced p38 MAPK activation is mediated by protein kinase A rather than by G(i) or G beta gamma in adult mouse cardiomyocytes
作者: Zheng, M; Zhang, SJ; Zhu, WZ; Ziman, B; Kobilka, BK; Xiao, RP
刊名: JOURNAL OF BIOLOGICAL CHEMISTRY
发表日期: 2000-12-22
卷: 275, 期:51, 页:40635-40640
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology
研究领域[WOS]: Biochemistry & Molecular Biology
关键词[WOS]: N-TERMINAL KINASES ; CARDIAC MYOCYTES ; TYROSINE KINASE ; STRESS ; HEART ; HYPERTROPHY ; STIMULATION ; SPECIFICITY ; INVOLVEMENT ; PHOSPHATASE
英文摘要:

Increasing evidence shows that stimulation of p-adrenergic receptor (AR) activates mitogen-activated protein kinases (MAPKs), in addition to the classical G(s) adenylyl cyclase-cAMP-dependent protein kinase (PKA) signaling cascade. In the present study, we demonstrate a novel beta (2)-AR-mediated cross-talk between PKA and p38 MAPK in adult mouse cardiac myocytes expressing beta (2)-AR, with a null background of beta (1)beta (2)-AR double knockout. beta (2)-AR stimulation by isoproterenol increased p38 MARK activity in a time- and dose-dependent manner. Inhibiting G(i) with pertussis toxin or scavenging G beta gamma with beta ARK-ct overexpression could not prevent beta (2)-AR-induced p38 MAPK activation. In contrast, a specific peptide inhibitor of PKA, PKI (5 muM), completely abolished the stimulatory effect of beta (2)-AR, suggesting that beta (2)-AR-induced p38 MAPK activation is mediated via a PKA-dependent mechanism, rather than by G(i) or G beta gamma. This conclusion was further supported by the ability of forskolin (10 muM), an adenylyl cyclase activator, to elevate p38 MAPK activity in a PKI-sensitive manner. Furthermore, inhibition of p38 MAPK with SB203580 (10 muM) markedly enhanced the beta (2)-AR-mediated contractile response, without altering base-line contractility. These results provide the first evidence that cardiac beta (2)-AR activates p38 MAPK via a PKA-dependent signaling pathway, rather than by G(i) or G beta gamma, and reveal a novel role of p38 MAPK in regulating cardiac contractility.

语种: 英语
WOS记录号: WOS:000166039500112
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/54953
Appears in Collections:北京大学第三临床医学院_心血管内科_期刊论文

Files in This Item:

There are no files associated with this item.


作者单位: 1.NIA, Gerontol Res Ctr, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA
2.Stanford Univ, Med Ctr, Howard Hughes Med Inst, Stanford, CA 94305 USA
3.Peking Univ, Hosp 3, Sch Med, Inst Vasc Med, Beijing 100083, Peoples R China

Recommended Citation:
Zheng, M,Zhang, SJ,Zhu, WZ,et al. beta(2)-adrenergic receptor-induced p38 MAPK activation is mediated by protein kinase A rather than by G(i) or G beta gamma in adult mouse cardiomyocytes[J]. JOURNAL OF BIOLOGICAL CHEMISTRY,2000,275(51):40635-40640.
Service
Recommend this item
Sava as my favorate item
Show this item's statistics
Export Endnote File
Google Scholar
Similar articles in Google Scholar
[Zheng, M]'s Articles
[Zhang, SJ]'s Articles
[Zhu, WZ]'s Articles
CSDL cross search
Similar articles in CSDL Cross Search
[Zheng, M]‘s Articles
[Zhang, SJ]‘s Articles
[Zhu, WZ]‘s Articles
Related Copyright Policies
Null
Social Bookmarking
Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit

Items in IR are protected by copyright, with all rights reserved, unless otherwise indicated.

 

 

Valid XHTML 1.0!
Copyright © 2007-2017  北京大学医学部 - Feedback
Powered by CSpace