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Immunoreactive macrophage colony‐stimulating factor is increased in atherosclerotic lesions of watanabe heritable hyperlipidemic rabbits after recombinant human macrophage colony‐stimulating factor therapy
Author(s) -
Donnelly Lori Hayes,
Bree Mark P.,
Hunter Sharon E.,
Keith James C.,
Schaub Robert G.
Publication year - 1997
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/(sici)1098-2795(199701)46:1<92::aid-mrd14>3.0.co;2-5
Subject(s) - biology , macrophage colony stimulating factor , macrophage , foam cell , monocyte , colony stimulating factor , recombinant dna , cholesterol , immunology , endocrinology , medicine , lipoprotein , microbiology and biotechnology , in vitro , biochemistry , gene , stem cell , haematopoiesis
Infiltration of monocytes into arteries is an early event in the pathogenesis of atherosclerosis. This recruitment is interpreted as enhancing lesion development, but it could also be a host response limiting lipid accumulation. The ability of macrophages to limit cholesterol uptake, however, can be reduced by the impaired mobility and metabolic activity associated with foam cell development. As lesions enlarge, foam cells die and become the nidus for the necrotic core. Treatments to improve viability might improve foam cell function and promote regression. Macrophage colony‐stimulating factor (M‐CSF) is vital to monocyte/macrophage differentiation, proliferation, and activation. We found that foam cells of Watanabe heritable hyperlipidemic (WHHL) rabbits had faint staining for M‐CSF. Treatment of rabbits with recombinant human M‐CSF (rhM‐CSF) increased M‐CSF staining, which correlated with reduced cholesterol content of these foam cells. Mol Reprod Dev 46:92–95, 1997. © 1997 Wiley‐Liss, Inc.