The role of miRNA-339-5p in the function of vascular endothelial progenitor cells in patients with PCOS.

RESEARCH QUESTION:miRNA-339 participates in diseases with endothelial progenitor cell (EPC) dysfunction. What is the role of miRNA-339-5p in EPC of polycystic ovary syndrome (PCOS)? DESIGN:Clinical data were collected from 76 controls and 84 PCOS patients. Noradrenaline, asymmetric dimethylarginine (ADMA), advanced glycation end products (AGE) and silent information regulator 1 (SIRT1) in the serum were measured. The functions of EPC and the expressions of PI3K, AKT, SIRT1 and PGC-1α in EPC before and after transfection with miRNA-339-5p mimic or miRNA-339-5p inhibitor were compared. RESULTS:Serum concentrations of noradrenaline, ADMA and AGE were significantly higher (P = 0.009, P = 0.044, P < 0.001) and the SIRT1 concentration was significantly lower (P < 0.001) in PCOS patients, especially obese ones (P = 0.034, P = 0.032, P < 0.001, P = 0.023) than in the control group. When compared with the controls, proliferation of the EPC was slightly lower (without a significant difference), the migration and tubular formation were significantly decreased (P = 0.037, P = 0.011), the expression of miRNA-339-5p in EPC was significantly higher (P = 0.035) and the expressions of PI3K, AKT, SIRT1 and PGC-1α were significantly lower in the PCOS group (mRNA: P = 0.033, P = 0.027, P = 0.027, P = 0.032; protein: P = 0.036, P = 0.028, P = 0.039, P = 0.023). After transfection, the functions of EPC from PCOS patients were best in the miRNA-339-5p inhibitor group, and weakest in the miRNA-339-5p mimic group. The miRNA-339-5p inhibitor group had higher protein expressions of PI3K, AKT and SIRT1 but lower expression of PGC-1α in PCOS patients (P < 0.001, P = 0.030, P = 0.047, P = 0.003). Similar results were obtained from the controls after transfection. CONCLUSION:Increased sympathetic excitation and damage to EPC were observed in PCOS patients, especially obese ones. Up-regulated miRNA-339-5p could inhibit the function of EPC by inhibiting the PI3K/AKT and SIRT1/PGC-1α signalling pathways.