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Role of macrophage colony-stimulating factor in the development of neointimal thickening following arterial injury.
Mishra, Vivek; Sinha, Satyesh K; Rajavashisth, Tripathi B.
Afiliação
  • Mishra V; Molecular Biology Unit, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, India.
  • Sinha SK; Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059, USA.
  • Rajavashisth TB; Molecular Biology Unit, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, India; Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059, USA; David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA 90095, USA. Electronic address: rajavashisth@ucla.edu.
Cardiovasc Pathol ; 25(4): 284-292, 2016.
Article em En | MEDLINE | ID: mdl-27135205
Evidence suggests that macrophage colony-stimulating factor (M-CSF) participates critically in atherosclerosis; little is known about the role of M-CSF in the development of neointimal hyperplasia following mechanical vascular injury. We examined the expression of M-CSF and its receptor, c-fms, in rodent and rabbit models of arterial injury. Injured rat carotid arteries expressed 3- to 10-fold higher levels of M-CSF and c-fms mRNA and protein following balloon injury as compared to uninjured arteries. In the rabbit, M-CSF protein expression was greatest in neointimal smooth muscle cells (SMCs) postinjury, with some expression in medial SMCs. M-CSF-positive SMCs exhibited markers of proliferation. At 30days postinjury, neointimal SMCs in the adjacent healed area near the border between injured and uninjured zone lost both proliferative activity and overexpression of M-CSF. The presence of induced M-CSF and c-fms expression correlated with the initiation of SMCs proliferation. M-CSF stimulated incorporation of [(3)H] thymidine in human aortic smooth muscle cells in a concentration-dependent manner. Serum-free conditioned medium from aortic SMCs also promoted DNA synthesis, and this effect was blocked by M-CSF specific antibody. To test further the role of M-CSF in vivo, we induced arterial injury by placing a periadventitial collar around the carotid arteries in compound mutant mice lacking apolipoprotein apoE (apoE(-/-)) and M-CSF. Loss of M-CSF abolished the neointimal hyperplastic response to arterial injury in apoE(-/-) mice. Local delivery of M-CSF to the injured artery restored neointimal proliferation, suggesting a critical role of M-CSF for the development of neointimal thickening following arterial injury.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fator Estimulador de Colônias de Macrófagos / Lesões das Artérias Carótidas / Neointima Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Cardiovasc Pathol Assunto da revista: ANGIOLOGIA / CARDIOLOGIA / PATOLOGIA Ano de publicação: 2016 Tipo de documento: Article País de afiliação: Índia País de publicação: Estados Unidos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fator Estimulador de Colônias de Macrófagos / Lesões das Artérias Carótidas / Neointima Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Cardiovasc Pathol Assunto da revista: ANGIOLOGIA / CARDIOLOGIA / PATOLOGIA Ano de publicação: 2016 Tipo de documento: Article País de afiliação: Índia País de publicação: Estados Unidos