Overexpression of wild-type Gαi-2 suppresses β-adrenergic signaling in cardiac myocytes
Overexpression of wild-type Gαi-2 suppresses β-adrenergic signaling in cardiac myocytes
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DOI：
10.1096/fj.02-0660fje
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发表时间：
2003-01-01
期刊：
影响因子：
4.8
通讯作者：
Eschenhagen, T
中科院分区：
文献类型：
--
作者：
Rau, T;Nose, M;Eschenhagen, T
Galphai-2过表达在心力衰竭中β-肾上腺素能信号脱敏中的作用是有争议的。使用基于腺病毒的方法来研究Galphai-2的过表达是否损害新生大鼠心肌细胞（NRCM）中腺苷酸环化酶（AC）活性和cAMP水平的β-肾上腺素能刺激以及成年大鼠心室肌细胞（ARVM）的细胞缩短。用Ad 5Galphai-2感染NRCM以病毒剂量依赖性方式使Galphai-2增加50-600%。抑制GTP和异丙肾上腺素刺激的AC 10-72%（P
The role of Galphai-2 overexpression in desensitization of beta-adrenergic signaling in heart failure is controversial. An adenovirus-based approach was used to investigate whether overexpression of Galphai-2 impairs beta-adrenergic stimulation of adenylyl cyclase (AC) activity and cAMP levels in neonatal rat cardiac myocytes (NRCM) and cell shortening of adult rat ventricular myocytes (ARVM). Infection of NRCM with Ad5Galphai-2 increased Galphai-2 by 50-600% in a virus dose-dependent manner. Overexpression was paralleled by suppression of GTP- and isoprenaline-stimulated AC by 10-72% (P