ROLE OF CIRCULATING ENDOTHELIAL PROGENITOR CELLS AND CORRELATION WITH VASCULAR STIFFNESS AND ORGAN DAMAGE

Objective Atherosclerosis is a chronic cardiovascular disease. High plasma concentration of LDL is the main risk factor but the role of inflammation in all the stages become recently evident. Atherosclerosis and lipid metabolism change according to gender differences. Several possible markers of endothelial dysfunction and vascular stiffness have been identified, including clinical-instrumental and biochemical markers of inflammation and/or fibrosis (i.e., TNF-alpha, prostaglandin, L-Arginine/Asymmetric dimethylarginine - ADMA). A common mechanism identified in the pathogenesis of numerous CVD is endothelial dysfunction that correlates with circulating endothelial progenitor cells (EPCs). These cells are recruited from the bone marrow in response to vascular damage or tissue ischemia. In the peripheral blood, EPCs contribute to reendothelialization and neovascularization, acting as positive regulators of hemostasis and vascular integrity. A reduction in their number or function has been correlated to progression of CVD and MACE. Our project aims to assess the role of EPCs and L-ARG/ADMA in arterial stiffness and atherosclerosis. Design and method Our study is a prospective experimental investigation, enrolling all patients with cardiovascular disease. Patients will undergo routine hematological and biochemical tests as well as instrumental examinations in accordance with good clinical practice. The enrolled patients will undergo a series of clinical and instrumental examinations (ABI,PWV). In in vitro experiments, EPCs will be isolated from PBMCs and functional assays will be performed. Also, Proteome Profiler Target Analytes study and ELISA assay (L-Arg/ADMA) will be performed. Results There was a direct correlation between SCORE2/2-OP and PWV (r=0.70; p<0.0001). Preliminary data indicated a correlation between L-Arg/ADMA to SCORE2/2OP (r=0.36, p=0.04), Total Cholesterol (r=0.75, p=0.033) and LDL (r=0.75, p=0.031), as well as EPCs and their migration correlates to a change in folate cycle (P<0.007 Conclusions preliminary data suggests the importance of EPCs as specific read-out of cell activation and tissue damage in response to cardiovascular risk factors.