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TISSUE-SPECIFIC STEM CELLS

Mechanisms Underlying Acceleration of Blood Flow Recovery in Ischemic Limbs by Macrophage Colony-Stimulating Factor

^a First Department of Pathology,
^b Department of Pediatrics,
^c Regeneration Research Center for Intractable Diseases, Kansai Medical University, Moriguchi, Osaka, Japan

Key Words. Macrophage colony-stimulating factor • Vascular endothelial growth factor • Neovascularization • Endothelial progenitor cell

Correspondence: Susumu Ikehara, M.D., Ph.D., First Department of Pathology, Kansai Medical University, 10-15 Moriguchi, Osaka, Japan. Telephone: 81-66-993-1001 ex. 2470; Fax: 81-66-994-8283; e-mail ikehara{at}takii.kmu.ac.jp

Received August 29, 2005; accepted for publication January 22, 2006.
Recently we reported that macrophage colony-stimulating factor (M-CSF) can mobilize endothelial progenitor cells (EPCs) from the bone marrow into the peripheral blood, resulting in an increase in the number of blood vessels and augmentation of blood flow in the ischemia-induced legs. M-CSF accelerates neovascularization of ischemic lesions resulting from the mobilization of EPCs. In the present paper, we analyze the mechanisms underling the mobilization of EPCs by M-CSF. M-CSF augments the production of vascular endothelial growth factor (VEGF) from the bone marrow cells, especially from myeloid lineage cells. In vivo administration of anti-VEGF antibody abrogates both the acceleration of the recovery of blood flow in the ischemia-induced limbs by M-CSF and the augmentation of the mobilization of EPCs induced by M-CSF. These results suggest that the M-CSF contributes to rapid recovery of blood flow in ischemic lesions by mobilization of EPCs from the bone marrow through augmentation of VEGF production in the bone marrow and that the VEGF is mainly produced by myeloid lineage cells.