Author: ["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"]
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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.Cite this article
Harada, M., Qin, Y., Takano, H. et al. G-CSF prevents cardiac remodeling after myocardial infarction by activating the Jak-Stat pathway in cardiomyocytes. Nat Med 11, 305–311 (2005). https://doi.org/10.1038/nm1199 