G-CSF Augments Small Vessel and Cell Density in Canine Myocardial Infarction

DOI Web Site 参考文献65件
  • Yagi Takashi
    Cardiopulmonary Division, Department of Internal Medicine, Keio University School of Medicine
  • Fukuda Keiichi
    Institute for Advanced Cardiac Therapeutics, Keio University School of Medicine
  • Fujita Jun
    Institute for Advanced Cardiac Therapeutics, Keio University School of Medicine
  • Endo Jin
    Cardiopulmonary Division, Department of Internal Medicine, Keio University School of Medicine
  • Hisaka Yasuyo
    Institute for Advanced Cardiac Therapeutics, Keio University School of Medicine
  • Suzuki Yoshiyuki
    Fuji Gotemba Research Labs, Chugai Pharmaceutical Co., Ltd.
  • Tamura Masahiko
    Chugai Research Institute for Medical Science, Inc.
  • Ogawa Satoshi
    Cardiopulmonary Division, Department of Internal Medicine, Keio University School of Medicine

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We recently reported that granulocyte-colony stimulating factor (G-CSF) prevented cardiac remodeling by mobilization and differentiation of bone marrow-derived cells in murine experimental myocardial infarction (MI). Little is known, however, whether these findings can be reproduced in large animals. The aim of this study is to investigate the effect of G-CSF after MI in canine model. MI was generated in twenty-six beagle dogs by ligation of left anterior descending artery. They were divided into two groups: G-CSF group which received subcutaneous injection of G-CSF (10 μg/kg/day) for 10 days, and the control group with saline injection. After six weeks, they were subjected to echocardiography and catheterization to measure hemodynamic parameters, and histological analysis was performed. No dogs died during the period. No hemodynamic changes were observed between these two groups probably due to the smaller size of the MI than we expected. We found significant increase in wall thickness and higher cell density in G-CSF group. Immunohistochemical staining against α-smooth muscle actin and CD31 revealed increased vessel density mainly in the epicardium in G-CSF group. The number of survived cardiomyocytes in G-CSF group was slightly greater than that in the control group, although it was not statistically significant. These findings suggested G-CSF prevented cardiac remodeling in canine model not by increasing the cardiomyocytes but by increasing the vessel density and cell numbers in the infarcted area.

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