EXPRESSION OF ADIPONECTIN RECEPTORS IN HUMAN CAROTID ATHEROSCLEROTIC PLAQUES Abstracts from the 12th National Congress of the Italian Society of Cardiovascular Prevention (SIPREC), Naples, 6–8 March 2014

Introduction: Adiponectin is a protein secreted by the adipose tissue with pleiotropic effects on metabolism. This adipokine play different anti-atherogenic action, such as the improvement of endothelial function and anti-inflammatory status in arterial walls. Two receptors ubiquitously expressed, AdipoR1 and AdipoR2, are involved in its action which. In obesity a mechanism of adiponectin resistance was demonstrated. Aim: To verify if adiponectin-resistance occurs in human atherosclerotic plaques. Methods: RNA from 49 carotid atherosclerotic plaques (advanced lesions), their respective adjacent regions (witha low grade lesions) and 7 healthy arteries (iliac and mesenteric) was extracted, reverse-transcribed and used for real-time PCR by specific TaqMan assays (Applied Biosystems). In vitro experiments for gene regulation studies were performed on primary Human Aortic Endothelial Cells and Smooth Muscle Cells (Lonza) co-cultured with the macrophage cell line THP-1. Results: Expression levels of AdipoR1 were lower in advanced plaques as well as in their respective adjacent regions than in healthy arteries (p = 0.020 and p = 0.001 respectively). AdipoR2 levels gradually decreased from healthy arteries to plaque adjacent regions and to advanced plaques (all comparisons p\0.0001). In both cell types, expression of AdipoR1 was not affected by the co-culture with THP-1. The presence of THP-1 decreased AdipoR2 expression in Smooth Muscle Cells (p = 0.040), whereas a not statistically significant decrease was observed in Endothelial Cells. Conclusions: We demonstrated a decreased expression of adiponectin receptors in initial and advanced plaques, suggesting a mechanism of adiponectin-resistance during atherosclerotic process. A local adiponectin-resistance could be a main cause of the lack of atheroprotective effects mediated by adiponectin. Presence of macrophages could be a contributory cause of AdipoR2 decrease.