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学科主题临床医学
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
Zheng, M; Zhang, SJ; Zhu, WZ; Ziman, B; Kobilka, BK; Xiao, RP
刊名JOURNAL OF BIOLOGICAL CHEMISTRY
2000-12-22
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
引用统计
被引频次:97[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/400002259/54953
专题北京大学第三临床医学院_心血管内科
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
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GB/T 7714
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.
APA Zheng, M,Zhang, SJ,Zhu, WZ,Ziman, B,Kobilka, BK,&Xiao, RP.(2000).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.JOURNAL OF BIOLOGICAL CHEMISTRY,275(51),40635-40640.
MLA Zheng, M,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".JOURNAL OF BIOLOGICAL CHEMISTRY 275.51(2000):40635-40640.
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