Granulocyte colony-stimulating factor activates Wnt signal to sustain gap junction function through recruitment of β-catenin and cadherin
Granulocyte colony-stimulating factor activates Wnt signal to sustain gap junction function through recruitment of β-catenin and cadherin
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DOI：
10.1016/j.febslet.2007.09.007
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发表时间：
2007-10-16
期刊：
影响因子：
3.5
通讯作者：
Sato, Takayuki
中科院分区：
文献类型：
--
作者：
Kuwabara, Masanorl;Kakinuma, Yoshihiko;Sato, Takayuki
我们之前的研究表明，ACh靶向连接蛋白（Cx） 43预防致死性心律失常。粒细胞集落刺激因子（G-CSF），用于治疗缺血性心力衰竭，可能是另一个候选，但机制未知。因此，我们研究了G-CSF的细胞效应。G-CSF激活心肌细胞中的Wnt和Jak2信号，上调Cx43蛋白和磷酸化水平。此外，G-CSF增强了Cx43、β -catenin和cadherin在质膜上的定位。G-CSF通过增强Cx43锚定抑制Cx43的减少，维持缺氧时细胞间的通讯。因此，GCSF抑制心肌梗死引起的室性心律失常。因此，G-CSF可作为心律失常的治疗工具。(c) 2007年欧洲生化学会联合会。Elsevier B.V.版权所有。
Our previous study reveals that connexin (Cx) 43 is targeted by ACh to prevent lethal arrhythmia. Granulocyte colony-stimulating factor (G-CSF), used against ischemic heart failure, may be another candidate, however, with unknown mechanisms. Therefore, we investigated the cellular effects of G-CSF. G-CSF activated the Wnt and Jak2 signals in cardiomyocytes, and up-regulated Cx43 protein and phosphorylation levels. In addition, G-CSF enhanced the localization of Cx43, beta-catenin and cadherin on the plasma membrane. G-CSF inhibited the reduction of Cx43 by enhancing Cx43 anchoring and sustained the cell-cell communication during hypoxia. Consequently, GCSF suppressed ventricular arrhythmia induced by myocardial infarction. As a result, G-CSF could be used as a therapeutic tool for arrhythmia. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.