| Title | Regulation of gap-junction protein connexin 43 by beta-adrenergic receptor stimulation in rat cardiomyocytes |
| Authors | Xia, Yi Gong, Kai-zheng Xu, Ming Zhang, You-yi Guo, Ji-hong Song, Yao Zhang, Ping |
| Affiliation | Peking Univ, Hosp 3, Inst Vasc Med, Beijing 100191, Peoples R China. Peking Univ, Peoples Hosp, Dept Cardiol, Electrophysiol Lab, Beijing 100044, Peoples R China. |
| Keywords | connexin43 gap junction beta-adrenergic receptor cardiac myocyte CARDIAC MYOCYTES KINASE-A MICE EXPRESSION CONDUCTION AGONISTS PHOSPHORYLATION HYPERTROPHY ARRHYTHMIAS SALBUTAMOL |
| Issue Date | 2009 |
| Publisher | 中国药理学报 |
| Citation | ACTA PHARMACOLOGICA SINICA.2009,30,(7),928-934. |
| Abstract | 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. |
| URI | http://hdl.handle.net/20.500.11897/307513 |
| ISSN | 1671-4083 |
| DOI | 10.1038/aps.2009.92 |
| Indexed | SCI(E) PubMed 中国科技核心期刊(ISTIC) 中国科学引文数据库(CSCD) |
| Appears in Collections: | 第三医院 人民医院 |
