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Immunohistochemical detection of macrophage‐derived foam cells and macrophage colony‐stimulating factor in pulmonary atherogenesis of cholesterol‐fed rabbits
Author(s) -
Ruan Yingmao,
Takahashi Kiyoshi,
Naito Makoto
Publication year - 1995
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/j.1440-1827.1995.tb03441.x
Subject(s) - foam cell , macrophage , pathology , immunohistochemistry , macrophage colony stimulating factor , monocyte , population , chemistry , biology , microbiology and biotechnology , medicine , immunology , in vitro , biochemistry , environmental health
In order to investigate the role of monocyte/macrophages and their relationship to the expression of macrophage colony‐stimulating factor (MCSF) in pulmonary atherosclerosis, lungs were excised from rabbits that had been fed for 60 and 90 days on a diet containing 0.5% cholesterol. In the lungs, fatty streaks and elevated foam cell lesions predominated in the large or medium‐sized elastic pulmonary arteries, while massive accumulation of foam cells in the intima of muscular arteries produced marked luminal narrowing and nearly complete occlusion. In these lesions, most of the foam cells were reactive with RbM2, a monoclonal antibody (mAb) against rabbit macrophages, while smooth muscle cell‐derived foam cells were detected by mAb against smooth muscle actin in the deeper area of elevated foam cell lesions of elastic arteries. Ultrastructural observation confirmed the presence of monocytes in the intima, their differentiation into macrophages, and their transformation into foam cells in the atherosclerotic lesions. lmmunohistochemical expression of MCSF was demonstrated in the endothelial cells, smooth muscle cells and foam cells. A minor macrophagederived foam cell population was demonstrated to possess a prolif‐erative capacity. These data suggest that MCSF is involved in the differentiation of monocytes into macrophages, their transformation into foam cells, and their proliferation during pulmonary atherogenesis.