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The novel adipokine chemerin significantly increases cholesterol uptake in human macrophages
Author(s) -
McCarthy Tanya C.,
Zuniga Luis A,
Zabel Brian A,
Butcher Eugene C,
Sinal Christopher J
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.948.8
Subject(s) - chemerin , adipokine , macrophage , foam cell , cholesterol , endocrinology , efflux , medicine , monocyte , chemistry , receptor , chemokine , biology , biochemistry , lipoprotein , in vitro , leptin , obesity
Atherosclerosis is the most common pathology underlying cardiovascular disease. One of the early events in atherosclerotic plaque formation is the excessive accumulation of cholesterol by macrophages leading to the development of macrophage foam cells. The novel adipokine chemerin is an endogenous ligand for CMKLR1, a G‐protein‐coupled receptor that is highly expressed on macrophage cells. Therefore, we hypothesized that chemerin may have an important role in the pathology of atherosclerosis through the modulation of macrophage function. Cholesterol uptake and efflux experiments show a significant increase in total cholesterol in human monocyte derived macrophages (MDM) treated with chemerin. Conversely chemerin treatment had no effect on cholesterol efflux in human MDM. Interestingly, the PPAR gamma ligand rosiglitazone, caused an increase in cholesterol efflux from human MDM with a corresponding decrease in the expression of CMKLR1. These data suggest that chemerin may play a role in macrophage cholesterol uptake and foam cell formation. Supported by the Canadian Institutes of Health Research and the National Institutes of Health