Statin therapy in hypertensive patients improved endothelial progenitor cell availability and migration, and reduced EPC-promoted microvascular density (19.8% vs 35.8%) compared to no statins.
Observational (n=75)
Does statin therapy improve endothelial progenitor cell function and modulate microRNA expression in hypertensive patients?
Statin therapy in hypertensive patients is associated with improved endothelial progenitor cell availability and migration, along with distinct miRNA signatures, suggesting a mechanism for vascular protection beyond lipid lowering.
Absolute Event Rate: 19.8% vs 35.8%
Abstract Background/Introduction Statins prevent atherosclerosis progression and reduce cardiovascular risk not only through lipid lowering but also by modulating vascular inflammation and endothelial dysfunction. Endothelial progenitor cells (EPCs), mobilized from bone marrow in response to vascular injury, contribute to endothelial repair, and alterations in their number or function reflect early vascular damage. miRNAs regulate key vascular processes, including inflammation and angiogenesis, and may mediate some vascular effects of statins. Recent studies have highlighted the role of statins in modulation of specific miRNAs involved in endothelial processes. For instance, lovastatin inhibits the aberrant expression of miR-133a, improving endothelial function. Similarly, statins-mediated upregulation of miR-29b reduces oxidative stress and prevents endothelial impairment in animal models with cardiovascular risk factors. Purpose To evaluate whether statin therapy may contribute to EPC functional properties associated to microRNA expression profiles in hypertensive 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 tests and instrumental examinations. EPCs were isolated for quantitative flow-cytometric analysis and migration assays. Small RNA sequencing identified differentially expressed miRNAs. Angiogenic behaviour was quantified using the chorioallantoic membrane assay (CAM). Statistical significance was set at P0.05. Results As expected, total cholesterol (160.3±30.5 vs 183.43±34.1 mg/dL, p=0.005) and LDL levels (83.5±31.4 vs 114.2±30.1 mg/dL, p=0.001) were lower in STAT (vs NO-STAT) patients. Concomitantly, statin treatement ameliorated EPC number and function. Flow cytometry showed that circulating CD133+CD34+VEGF+ EPCs were roughly an order of magnitude higher in STAT-treated than in NO-STAT patients, indicating increased availability of phenotypic EPCs. In wound-healing assays, EPCs from STAT-treated patients exhibited an approximately two-fold increase in migration ability compared with EPCs from NO-STAT patients. Small RNA sequencing revealed lower expression of miR-3960, miR-328-3p and miR-10400-5p in NO-STAT versus STAT-treated patients. Results from CAM suggest that EPCs from STAT-treated patients were less inclined to promote microvascular density (19.8% vs 35.8%), consistent with a more balanced angiogenically active endothelial phenotype. Conclusion(s) Statin therapy results in improved EPC availability and migration, associated with distinct EPC-derived miRNA signatures of vascular inflammation and angiogenesis. These findings support a modulatory interaction between statins, EPC biology and miRNA regulation, and may help to identify EPC-derived miRNA patterns as promising biomarkers of vascular status in hypertension.
Marozzi et al. (Fri,) conducted a observational in Hypertension (n=75). Statin therapy vs. No statin therapy was evaluated on Microvascular density promoted by EPCs. Statin therapy in hypertensive patients improved endothelial progenitor cell availability and migration, and reduced EPC-promoted microvascular density (19.8% vs 35.8%) compared to no statins.