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学科主题临床医学
Regulation of gap-junction protein connexin 43 by beta-adrenergic receptor stimulation in rat cardiomyocytes
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
2009-07-01
DOI10.1038/aps.2009.92
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
WOS记录号WOS:000268066400007
项目编号2006CB503806 ; 2007CB512008 ; 30471916 ; 30821001 ; 7052045
资助机构National Key Basic Research Program (NKBRP) of People&prime ; s Republic of China ; National Natural Science Foundation of China ; Beijing Municipal Natural Science Foundation
引用统计
被引频次:15[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/400002259/64427
专题北京大学临床肿瘤学院_药剂科
北京大学第三临床医学院_心血管内科
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
推荐引用方式
GB/T 7714
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.
APA Xia, Yi.,Gong, Kai-zheng.,Xu, Ming.,Zhang, You-yi.,Guo, Ji-hong.,...&Zhang, Ping.(2009).Regulation of gap-junction protein connexin 43 by beta-adrenergic receptor stimulation in rat cardiomyocytes.ACTA PHARMACOLOGICA SINICA,30(7),928-934.
MLA Xia, Yi,et al."Regulation of gap-junction protein connexin 43 by beta-adrenergic receptor stimulation in rat cardiomyocytes".ACTA PHARMACOLOGICA SINICA 30.7(2009):928-934.
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