CD36 in Atherosclerotic Coronary Artery Disease: Correlation with Angiogenesis and Inflammation

Background: CD36 is one of the macrophage scavenger receptor that has been implicated as a key player in the pathogenesis of atherosclerosis.Aim: This study focused on the role of CD36 in coronary artery disease (CAD) and its association with proangiogenic and inflammatory mediators. Patients and Methods:We studied 100 atherosclerotic CAD patients and 100 healthy controls.All patients had angiographic evidence of stenosis ≥ 50% in at least one major coronary artery Soluble CD36 (sCD36), peripheral blood mononuclear cells (PBMC-cCD36), vascular endothelial and platelet-derived growth factors (VEGF & PDGF), Tumor necrosis factor (TNF-α) and cycloxygenase-2 (COX-2) were measured using enzyme-linked immunosorbent assay (ELISA).CD36 mRNA expression was measured using reverse transcriptase polymerase chain reaction (RT-PCR).Results: A significant reduction in cCD36 expression (protein and mRNA) and plasma levels of sCD36, VEGF, PDGF in CAD patients was demonstrated.In contrast, a marked elevation in the plasma level of TNF-α was observed.There was a strong inverse correlation between severity of CAD and sCD36 (r = -0.413;P < 0.001), cCD36 (r = -0.4663;P < 0.001), CD36 mRNA (r = -0.328;P < 0.01).Furthermore, CD36 was found to be positively correlated with VEGF (r = 0.446; P < 0.001) and PDGF (r = 0.287; P < 0.05), while it was negatively correlated with TNF-α (r= -0.352; P < 0.01).Conclusion: CD36 deficiency might represent a good expression marker for the development of CAD in Egyptian patients in association with inflammatory and proangiogenic mediators.Targeting the underling mechanism of the direct and inverse association of CD36 with angiogenic and inflammatory mediators could be used in the treatment of athero-inflammatory disorders.