G-CSF prevents cardiac remodeling after myocardial infarction by activating the Jak-Stat pathway in cardiomyocytes View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2005-02-20

AUTHORS

Mutsuo Harada, Yingjie Qin, Hiroyuki Takano, Tohru Minamino, Yunzeng Zou, Haruhiro Toko, Masashi Ohtsuka, Katsuhisa Matsuura, Masanori Sano, Jun-ichiro Nishi, Koji Iwanaga, Hiroshi Akazawa, Takeshige Kunieda, Weidong Zhu, Hiroshi Hasegawa, Keita Kunisada, Toshio Nagai, Haruaki Nakaya, Keiko Yamauchi-Takihara, Issei Komuro

ABSTRACT

Granulocyte colony-stimulating factor (G-CSF) was reported to induce myocardial regeneration by promoting mobilization of bone marrow stem cells to the injured heart after myocardial infarction, but the precise mechanisms of the beneficial effects of G-CSF are not fully understood. Here we show that G-CSF acts directly on cardiomyocytes and promotes their survival after myocardial infarction. G-CSF receptor was expressed on cardiomyocytes and G-CSF activated the Jak/Stat pathway in cardiomyocytes. The G-CSF treatment did not affect initial infarct size at 3 d but improved cardiac function as early as 1 week after myocardial infarction. Moreover, the beneficial effects of G-CSF on cardiac function were reduced by delayed start of the treatment. G-CSF induced antiapoptotic proteins and inhibited apoptotic death of cardiomyocytes in the infarcted hearts. G-CSF also reduced apoptosis of endothelial cells and increased vascularization in the infarcted hearts, further protecting against ischemic injury. All these effects of G-CSF on infarcted hearts were abolished by overexpression of a dominant-negative mutant Stat3 protein in cardiomyocytes. These results suggest that G-CSF promotes survival of cardiac myocytes and prevents left ventricular remodeling after myocardial infarction through the functional communication between cardiomyocytes and noncardiomyocytes. More... »

PAGES

305-311

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nm1199

DOI

http://dx.doi.org/10.1038/nm1199

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1031699938

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/15723072


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