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Originally published online as doi:10.2353/ajpath.2007.061276 on July 19, 2007

Published online before print July 19, 2007
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(American Journal of Pathology. 2007;171:755-766.)
© 2007 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2007.061276

Bone Marrow-Derived CXCR4+ Cells Mobilized by Macrophage Colony-Stimulating Factor Participate in the Reduction of Infarct Area and Improvement of Cardiac Remodeling after Myocardial Infarction in Mice

Hajime Morimoto*, Masafumi Takahashi{dagger}, Yuji Shiba{dagger}, Atsushi Izawa{dagger}, Hirohiko Ise{dagger}, Minoru Hongo{ddagger}, Kiyohiko Hatake§, Kazuo Motoyoshi and Uichi Ikeda*{dagger}

From the Department of Cardiovascular Medicine and Regeneration* and the Division of Cardiovascular Sciences,{dagger} the Department of Organ Regeneration, Shinshu University Graduate School of Medicine, Matsumoto; the Department of Cardiovascular Medicine,{ddagger} Shinshu University School of Health Sciences, Matsumoto; the Cancer Chemotherapy Center,§ Japanese Foundation for Cancer Research, Tokyo; and the Third Department of Internal Medicine, National Defense Medical College, Saitama, Japan

The monocyte/macrophage lineage might affect the healing process after myocardial infarction (MI). Because macrophage colony-stimulating factor (M-CSF) stimulates differentiation and proliferation of this lineage, we examined the effect of M-CSF treatment on infarct size and left ventricular (LV) remodeling after MI. MI was induced in C57BL/6J mice by ligation of the left coronary artery. Either recombinant human M-CSF or saline was administered for 5 consecutive days after MI induction. M-CSF treatment significantly reduced the infarct size (P < 0.05) and scar formation (P < 0.05) and improved the LV dysfunction (percent fractional shortening, P < 0.001) after the MI. Immunohistochemistry revealed that M-CSF increased macrophage infiltration (F4/80) and neovascularization (CD31) of the infarct myocardium but did not increase myofibroblast accumulation ({alpha}-smooth muscle actin). M-CSF mobilized CXCR4+ cells into peripheral circulation, and the mobilized CXCR4+ cells were then recruited into the infarct area in which SDF-1 showed marked expression. The CXCR4 antagonist AMD3100 deteriorated the infarction and LV function after the MI in the M-CSF-treated mice. In conclusion, M-CSF reduced infarct area and improved LV remodeling after MI through the recruitment of CXCR4+ cells into the infarct myocardium by the SDF-1-CXCR4 axis activation; this suggests that the SDF-1-CXCR4 axis is as a potential target for the treatment of MI.






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Copyright © 2007 by the American Society for Investigative Pathology.