on October 19, 2006
Published online before print October 19, 2006, doi: 10.1161/01.ATV.0000250606.70669.14
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Submitted on July 24, 2006
Accepted on September 28, 2006
M-CSF Accelerates Neointimal Formation in the Early Phase After Vascular Injury in Mice. The Critical Role of the SDF-1-CXCR4 System
Yuji Shiba ;
From the Division of Cardiovascular Sciences, Department of Organ Regeneration (Y.S., M.T., T.Y., N.Y., H.M., A.I., H.I., U.I.), Shinshu University Graduate School of Medicine, Matsumoto; the Cancer Chemotherapy Center (K.H.), Japanese Foundation for Cancer Research, Tokyo; and the Third Department of Internal Medicine (K.M.), National Defense Medical College, Saitama, Japan.
* To whom correspondence should be addressed. E-mail: masafumi{at}sch.md.shinshu-u.ac.jp.
Objective--Since the macrophage CSF (M-CSF) has been shown to stimulate differentiation and proliferation of monocyte/macrophage lineage and to be involved in the process of neointimal formation after vascular injury, we tested the effects of M-CSF on the recruitment of bone marrow-derived progenitor cells in neointimal formation after vascular injury in mice.
Methods and Results--Wire-mediated vascular injury was produced in the femoral artery of C57BL/6 mice. Recombinant human M-CSF [500 µg/(kg·day)] or saline (control) was administered for 10 consecutive days, starting 4 days before the injury. Treatment with M-CSF accelerated neointimal formation in the early phase after injury, and this neointimal lesion mainly consisted of bone marrow-derived cells. M-CSF treatment had no effect on the mobilization of endothelial progenitor cells (EPCs: CD34+/Flk-1+) and reendothelialization after injury. The stromal cell-derived factor-1 (SDF-1) was markedly expressed in the neointima and media after injury, whereas CXCR4+ cells were observed in the neointima. Further, a novel CXCR4 antagonist, AMD3100, significantly attenuated the M-CSF-induced neointimal formation.
Conclusions--These findings suggest that M-CSF accelerated neointimal formation after vascular injury via the SDF-1-CXCR4 system, and the inhibition of this system has therapeutic potential for the treatment of cardiovascular diseases.
Key words: angioplasty • cytokines • inflammation • restenosis • vascular biology
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