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Am J Pathol ; 172(3): 839-48, 2008 Mar.
Article in English | MEDLINE | ID: mdl-18276778

ABSTRACT

Intimal hyperplasia of autologous vein grafts is a critical problem affecting the long-term patency of many types of vascular reconstruction. Within intimal hyperplasia lesions, smooth muscle cells are a major component, playing an essential role in the pathological process. Given that bone marrow-derived cells may differentiate into smooth muscle cells in the neointima of injured arteries, we hypothesized that the bone marrow may serve as a source for some of the smooth muscle cells within intimal hyperplasia lesions of vein grafts. To test this hypothesis, we used an established mouse model for intimal hyperplasia in wild-type mice that had been transplanted with bone marrow from a green fluorescent protein (GFP+/+) transgenic mouse. High-resolution confocal microscopy analysis performed 2 and 8 weeks after grafting demonstrated expression of GFP in 5.4 +/- 0.8% and 11.9 +/- 2.3%, respectively, of smooth muscle cells within intimal hyperplasia lesions. By 16 weeks, GFP expression in smooth muscle cells was not detected by immunohistochemistry; however, real-time PCR revealed that 20.2 +/- 1.7% of the smooth muscle cells captured from the neointima lesion by laser capture microdissection at 16 weeks contained GFP DNA. Our results suggest that bone marrow-derived cells differentiated into smooth muscle cells within the intimal lesion and may provide a novel clinical approach for decreasing intimal hyperplasia in vein grafts.


Subject(s)
Bone Marrow Transplantation/physiology , Tunica Intima/pathology , Veins/transplantation , Animals , Cell Proliferation , Green Fluorescent Proteins/genetics , Green Fluorescent Proteins/metabolism , Hyperplasia/therapy , Mice , Mice, Inbred C57BL , Mice, Transgenic , Microdissection , Myocytes, Smooth Muscle/metabolism , Myocytes, Smooth Muscle/physiology , Time Factors , Transplantation, Autologous , Treatment Outcome
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