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Abstract
Vascular smooth muscle cells in atherosclerotic lesions are phenotypically different from those in the normal arterial wall, and no expression of macrophage colony stimulating factor (M-CSF) receptor encoded by the proto-oncogene c-fms has been demonstrated in normal smooth muscle cells. In the present study, we demonstrated expression of c-fms and high affinity binding of M-CSF in smooth muscle cells isolated from an experimental rabbit model of arteriosclerosis (intimal smooth muscle cells), while no expression of c-fms was shown in medial smooth muscle cells. In the immunocytochemical analysis, both types of smooth muscle cells similarly reacted with an antibody specific to muscle cells (HHF 35) but did not react with an antibody specific to rabbit macrophages (RAM 11). In intimal smooth muscle cells, when cells were incubated with acetylated low density lipoproteins (LDL), the binding of acetylated LDL and foam cell formation were observed. In response to M-CSF, tyrosine-phosphorylation, as analyzed by the detection of anti-phosphotyrosine-reactive proteins, and an increased rate of cell proliferation were observed in intimal smooth muscle cells. These results indicated that intimal smooth muscle cells have the characteristics of monocyte-macrophages such as the expression of c-fms, which may be related to their proliferation and phenotypic conversion into foam cells in atheromatous lesions.
Highlights
1, interleukin-6, tumor necrosis factor a, interferons,and colony stimulating factors arereported to be synthesized and secreted by vascular cell components including endothelial cells, monocyte-macrophages, smooth muscle cells, and lymphocytes [3,4,5,6]
Smooth muscle cells migrate from Materials-Sodium [1251]iodidaend [3H]thymidinewere purchased the media tothe intima of thearterial wall, where they from ICN Radiochemicals. ‘“I-PDGF-BB homodimer was purchased proliferate and endocytose various lipoproteins including from Amersham
Smooth muscle cells was produced with Chinese hamster ovary cells transfected with the undergo structural and functional changes from a contractile to a syntheticphenotype [2]. the precise mechanism of the phenotypic change is not fully understood, various cytokines and growth factors are proposed to be involved in plasmid that contained the cDNA of M-CSF as previously described [8]
Summary
1, interleukin-6, tumor necrosis factor a, interferons,and colony stimulating factors arereported to be synthesized and secreted by vascular cell components including endothelial cells, monocyte-macrophages, smooth muscle cells, and lymphocytes [3,4,5,6]. Cells were incubated with rabbit smooth muscle cells was performed on multi-welledslides fixed 10 ng/ml M-CSF or 10 ng/ml PDGF for 5 min a t 4 "C. This indicated that the intimal smooth muscle cells that we isolated are immunologically different from macrophages,and biological activity using the method of Stanley [19].
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