STATINS CHANGE miRNA EXPRESSION IN CIRCULATING ENDOTHELIAL PROGENITOR CELLS FROM HYPERTENSIVE PATIENTS

Introduction: Statins are still one of the most common and effective treatments to prevent atherosclerosis progression. In addition to reducing high plasma concentration of LDL, statins may contribute to counteract vascular inflammation and endothelial disfunction in patients at cardiovascular (CV) risk. Endothelial dysfunction correlates to an impaired availability of circulating endothelial progenitor cells (EPCs), physiologically recruited from bone marrow in response to vascular damage. EPCs contribute to re-endothelialization and vascular integrity. Aim: We investigated whether statins might help to ameliorate EPCs number and function, therefore helping to elucidate potential additional mechanisms for statins protective effects on CV disease-prone patients. Methods: Hypertensive patients receiving (STAT, n = 51, 24F, aged 67.7 ± 9.6) or not (NO-STAT, n = 24, 13F, aged 63.1 ± 11.3) statin treatment underwent routine laboratory and instrumental examinations to assess arterial stiffness and organ damage (ABI, PWV). Quantitative and functional analysis was performed on EPCs isolated from patients of both groups. Small RNAseq was carried out to identify potential changes in microRNAs expression related to statin treatment. Statistical difference (p < 0.05) was considered significant. Results: PWV estimated vascular age was significantly higher in STAT (vs NO-STAT) patients. As expected, total cholesterol and LDL levels were lower in STAT (vs NO-STAT) patients. Interestingly, the total number of EPCs (by flow cytometry) and their ability to migrate (by wound healing assay) was significantly improved in STAT (vs NOSTAT) patients. Expression (by microRNAseq analysis) of miR-3960, mir-328-3p, mir-10400-5p, all involved in invasion and inflammation, was found downregulated in STAT (vs NO-STAT) patients. Conclusions: Preliminary findings suggest that the improved EPCs availability may represent an additional mechanism by which statins ameliorate vascular protection, likely dependent, at least in part, by modulation of specific microRNAs expression. Moreover, our findings emphasize the importance of EPCs as a potential