Granulocyte colony-stimulating factor activates Wnt signal to sustain gap junction function through recruitment of β-catenin and cadherin

Masanori Kuwabara, Yoshihiko Kakinuma, Rajesh G. Katare, Motonori Ando, Fumiyasu Yamasaki, Yoshinori Doi, Takayuki Sato

Research output: Contribution to journalArticle

31 Citations (Scopus)

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, β-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.

Original languageEnglish
Pages (from-to)4821-4830
Number of pages10
JournalFEBS Letters
Volume581
Issue number25
DOIs
Publication statusPublished - Oct 16 2007

Keywords

  • Cadherin
  • Connexin
  • Gap junction
  • Granulocyte-colony stimulating factor
  • Hypoxia
  • β-Catenin

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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