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TISSUE-SPECIFIC STEM CELLS |
aDepartment of Regenerative Medicine and Advanced Cardiac Therapeutics,
bDivision of Cardiology, Department of Internal Medicine,
cDepartment of Cardiac Surgery, and
dDepartment of Physiology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan;
eDepartment of Medicine and
fResearch Center for Regenerative Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan
Key Words. Myofibroblasts/fibroblasts • Monocytes/macrophages • Hematopoietic stem cells • Myocardial infarction Granulocyte colony-stimulating factor
Correspondence: Hiroshi Kawada, M.D., Ph.D., Department of Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1143, Japan. Telephone: 81-463-93-1121; Fax: 81-463-92-4511; e-mail: hkawada{at}is.icc.u-tokai.ac.jp; Keiichi Fukuda, Department of Regenerative Medicine and Advanced Cardiac Therapeutics, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Telephone: 81-3-5363-3874; Fax: 81-3-5363-3875; e-mail: kfukuda{at}sc.itc.keio.ac.jp
Received April 14, 2007;
accepted for publication July 27, 2007.
First published online in STEM CELLS EXPRESS August 9, 2007.
The administration of granulocyte colony-stimulating factor (G-CSF) after myocardial infarction (MI) improves cardiac function and survival rates in mice. It was also reported recently that bone marrow (BM)-derived c-kit+ cells or macrophages in the infarcted heart are associated with improvement of cardiac remodeling and function. These observations prompted us to examine whether BM-derived hematopoietic cells mobilized by G-CSF administration after MI play a beneficial role in the infarct region. A single hematopoietic stem cell from green fluorescent protein (GFP)-transgenic mice was used to reconstitute hematopoiesis in each experimental mouse. MI was then induced, and the mice received G-CSF for 10 days. In the acute phase, a number of GFP+ cells showing the elongated morphology were found in the infarcted area. Most of these cells were positive for vimentin and 
-smooth muscle actin but negative for CD45, indicating that they were myofibroblasts. The number of these cells was markedly enhanced by G-CSF administration, and the enhanced myofibroblast-rich repair was considered to lead to improvements of cardiac remodeling, function, and survival rate. Next, G-CSF-mobilized monocytes were harvested from the peripheral blood of GFP-transgenic mice and injected intravenously into the infarcted mice. Following this procedure, GFP+ myofibroblasts were observed in the infarcted myocardium. These results indicate that cardiac myofibroblasts are hematopoietic in origin and could arise from monocytes/macrophages. MI leads to the recruitment of monocytes, which differentiate into myofibroblasts in the infarct region. Administration of G-CSF promotes this recruitment and enhances cardiac protection. Disclosure of potential conflicts of interest is found at the end of this article.
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  J. Fransioli, B. Bailey, N. A. Gude, C. T. Cottage, J. A. Muraski, G. Emmanuel, W. Wu, R. Alvarez, M. Rubio, S. Ottolenghi, et al. Evolution of the c-kit-Positive Cell Response to Pathological Challenge in the Myocardium Stem Cells, May 1, 2008; 26(5): 1315 - 1324. [Abstract] [Full Text] [PDF]
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