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The aim of the current study was to determine the expression of microRNA (miRNA/miR)-329-3p in patients with type 2 diabetes mellitus (T2DM) and to investigate the effect of miR-329-3p on vascular endothelial cell function under high-glucose conditions. A total of 33 healthy individuals and 31 patients with T2DM were enrolled in the present study. Peripheral blood was collected from all participants. Human umbilical vein endothelial cells (HUVECs) were transfected with a miR-329-3p mimic or miR-329-3p inhibitor. Following treatment with 25 mmol/l glucose, a Cell Counting Kit-8 assay and flow cytometry analysis were used to assess cell viability and apoptosis levels, respectively. A dual luciferase reporter assay, western blot analysis and reverse transcription-quantitative PCR were used to assess molecular mechanism of miR-329-3p in HUVECs. The results revealed that plasma miR-329-3p expression was decreased patients with T2DM compared with healthy controls, and in HUVECs treated with high glucose concentrations. In addition, miR-329-3p reduced high glucose-induced damage to HUVEC cells. miR-329-3p directly bound to toll like receptor (TLR)-4 and regulated its expression at the transcriptional and post-transcriptional levels. miR-329-3p was also demonstrated to be involved in the regulation of the TLR4/tumor necrosis factor receptor associated factor 6 (TRAF6)/nuclear factor (NF)-κB signaling pathway and the nuclear translocation of NF-κB under a high glucose environment. In conclusion, the results indicated that miR-329-3p may protect endothelial cells from high glucose-induced apoptosis via inhibition of the TLR4/TRAF6/NF-κB signaling pathway. The present study also demonstrated that miR-329-3p expression in the plasma of patients with T2DM was reduced, suggesting that upregulation of miR-329-3p may alleviate high glucose-induced endothelial cell injury via inhibition of the TLR4/TRAF6/NF-κB signaling pathway.

MicroRNA‑329‑3p alleviates high glucose‑induced endothelial cell injury via inhibition of the TLR4/TRAF6/NF‑κB signaling pathway