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EP80317, a selective ligand of the CD36 scavenger receptor, reduces 111In‐labeled macrophages trafficking to atherosclerotic lesions in apoE‐deficient mice

Our recent studies have shown that long‐term (12 weeks) treatment with growth hormone‐releasing peptides (GHRPs), as ligands of the CD36 scavenger receptor, shows striking anti‐atherosclerotic effects in apoE‐deficient mice (apoE−/−) mice fed a high fat diet. Synthetic GHRPs such as hexarelin (Hex), in addition to binding CD36 on macrophages, also bind to the ghrelin receptor (GHS‐R1a). In order to assess the relative contribution of these receptors to fatty streak formation, apoE−/− mice have been treated with ghrelin, the endogenous GHS‐R1a ligand or with EP80317, a selective CD36 ligand. Long‐term treatment with ghrelin failed to modulate the development of aortic lesions whereas EP80317 was associated with a 51% reduction of lesions. Importantly, the effects of GHRPs were shown to be CD36‐dependent, no anti‐atherosclerotic effects were observed in apoE/CD36 double‐deficient mice. GHRP‐treated mice received 111In‐labeled macrophages and the aortic accumulation of labeled cells was assessed by radioactivity count of the aortic tree 48 hours later. Ghrelin failed to modulate 111In‐labeled macrophages accumulation within lesions whereas treatment with EP 80317 was associated with a 31 ± 6 % reduction of macrophages trafficking to atherosclerotic lesions, suggesting a potential role of EP80317 in modulating the inflammatory component of atherosclerosis. Our results suggest that GHRPs might be prototypes for a novel class of anti‐atherosclerotic agents.