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

doi:10.1016/j.febslet.2007.09.007

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 journal › Article › peer-review

32 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 language	English
Pages (from-to)	4821-4830
Number of pages	10
Journal	FEBS Letters
Volume	581
Issue number	25
DOIs	https://doi.org/10.1016/j.febslet.2007.09.007
Publication status	Published - 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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10.1016/j.febslet.2007.09.007

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

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.",

keywords = "Cadherin, Connexin, Gap junction, Granulocyte-colony stimulating factor, Hypoxia, β-Catenin",

author = "Masanori Kuwabara and Yoshihiko Kakinuma and Katare, {Rajesh G.} and Motonori Ando and Fumiyasu Yamasaki and Yoshinori Doi and Takayuki Sato",

note = "Funding Information: This study was supported by a Health and Labor Sciences Research Grant (H15-PHYSI-001) for Advanced Medical Technology from the Ministry of Health, Labor, and Welfare of Japan.",

year = "2007",

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doi = "10.1016/j.febslet.2007.09.007",

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AU - Kuwabara, Masanori

AU - Kakinuma, Yoshihiko

AU - Katare, Rajesh G.

AU - Ando, Motonori

AU - Yamasaki, Fumiyasu

AU - Doi, Yoshinori

AU - Sato, Takayuki

N1 - Funding Information: This study was supported by a Health and Labor Sciences Research Grant (H15-PHYSI-001) for Advanced Medical Technology from the Ministry of Health, Labor, and Welfare of Japan.

PY - 2007/10/16

Y1 - 2007/10/16

N2 - 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.

AB - 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.

KW - Cadherin

KW - Connexin

KW - Gap junction

KW - Granulocyte-colony stimulating factor

KW - Hypoxia

KW - β-Catenin

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

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Keywords

ASJC Scopus subject areas

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