Abstract
Endothelial cell senescence is closely related to the occurrence of cardiovascular diseases and microRNAs (miRNAs/miRs) are considered as therapeutic targets for cardiovascular disease. The current study aimed to investigate the role of miR‑20b in the senescence process of endothelial cells and its underlying mechanism. Cell viability, proportion of senescent cells and the cell cycle were respectively determined by Cell Counting Kit‑8, SA‑β‑galactosidase and flow cytometry. The relative expressions of mRNA and protein were detected by reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. The possible target genes and binding sites of miR‑20b were predicted using Targetscan and further verified by dual luciferase reporter assay. The present study found that H2O2 inhibited cell viability, caused cell cycle arrest in G1 phase, decreased miR‑20b level and induced cell senescence. Moreover, high expression of miR‑20b promoted cell viability and reduced H2O2‑induced cell senescence, whereas low expression of miR‑20b produced the opposite effects. Thioredoxin interacting protein (TXNIP) was predicted as a target gene for miR‑20b and knockdown of TXNIP increased cell viability, inhibited cell senescence, reduced the expression of p16, p21, TXNIP, NLR family pyrin domain containing 3 (NLRP3) and cleaved Caspase‑1 and reversed the promoting effects of the miR‑20b inhibitor and H2O2 on cell senescence. Furthermore, the knockdown of TXNIP inhibited the Wnt/β‑catenin pathway. The finding reveals that high expression of miR‑20b inhibits the senescence of human umbilical vein endothelial cells through regulating the Wnt/β‑catenin pathway via the TXNIP/NLRP3 axis.