Granulocyte colony-stimulating factor activates Wnt signal to sustain gap junction function through recruitment of beta-catenin and cadherin |
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Authors: | Kuwabara Masanori Kakinuma Yoshihiko Katare Rajesh G Ando Motonori Yamasaki Fumiyasu Doi Yoshinori Sato Takayuki |
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Affiliation: | Department of Medicine and Geriatrics, Kochi Medical School, Nankoku, Japan. |
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Abstract: | 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, G-CSF suppressed ventricular arrhythmia induced by myocardial infarction. As a result, G-CSF could be used as a therapeutic tool for arrhythmia. |
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Keywords: | Granulocyte-colony stimulating factor Connexin Hypoxia Cadherin β-Catenin Gap junction |
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