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学科主题: 临床医学
题名:
Regulation of gap-junction protein connexin 43 by beta-adrenergic receptor stimulation in rat cardiomyocytes
作者: Xia, Yi2; Gong, Kai-zheng1; Xu, Ming1; Zhang, You-yi1; Guo, Ji-hong2; Song, Yao1; Zhang, Ping2
关键词: connexin43 ; gap junction ; beta-adrenergic receptor ; cardiac myocyte
刊名: ACTA PHARMACOLOGICA SINICA
发表日期: 2009-07-01
DOI: 10.1038/aps.2009.92
卷: 30, 期:7, 页:928-934
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Chemistry, Multidisciplinary ; Pharmacology & Pharmacy
研究领域[WOS]: Chemistry ; Pharmacology & Pharmacy
关键词[WOS]: CARDIAC MYOCYTES ; KINASE-A ; MICE ; EXPRESSION ; CONDUCTION ; AGONISTS ; PHOSPHORYLATION ; HYPERTROPHY ; ARRHYTHMIAS ; SALBUTAMOL
英文摘要:

Aim: beta-adrenergic receptor (beta-AR) agonists are among the most potent factors regulating cardiac electrophysiological properties. Connexin 43 (Cx43), the predominant gap-junction protein in the heart, has an indispensable role in modulating cardiac electric activities by affecting gap-junction function. The present study investigates the effects of short-term stimulation of beta-AR subtypes on Cx43 expression and gap junction intercellular communication (GJIC) function.

Methods: The level of Cx43 expression in neonatal rat cardiomyocytes (NRCM) was detected by a Western blotting assay. The GJIC function was evaluated by scrape loading/dye transfer assay.

Results: Stimulation of beta-AR by the agonist isoproterenol for 5 min induces the up-regulation of nonphosphorylated Cx43 protein level, but not total Cx43. Selective beta(2)-AR inhibitor ICI 118551, but not beta(1)-AR inhibitor CGP20712, could fully abolish the effect. Moreover, pretreatment with both protein kinase A inhibitor H89 and G(i) protein inhibitor pertussis toxin also inhibited the isoproterenol-induced increase of nonphosphorylated Cx43 expression. Isoproterenol-induced up-regulation of nonphosphorylated Cx43 is accompanied with enhanced GJIC function.

Conclusion: Taken together, beta(2)-AR stimulation increases the expression of nonphosphorylated Cx43, thereby enhancing the gating function of gap junctions in cardiac myocytes in both a protein kinase A-and G(i)-dependent manner.

语种: 英语
所属项目编号: 2006CB503806 ; 2007CB512008 ; 30471916 ; 30821001 ; 7052045
项目资助者: National Key Basic Research Program (NKBRP) of People&prime ; s Republic of China ; National Natural Science Foundation of China ; Beijing Municipal Natural Science Foundation
WOS记录号: WOS:000268066400007
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/64427
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.Peking Univ, Peoples Hosp, Dept Cardiol, Electrophysiol Lab, Beijing 100044, Peoples R China

Recommended Citation:
Xia, Yi,Gong, Kai-zheng,Xu, Ming,et al. Regulation of gap-junction protein connexin 43 by beta-adrenergic receptor stimulation in rat cardiomyocytes[J]. ACTA PHARMACOLOGICA SINICA,2009,30(7):928-934.
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