MiR-217 alleviates high-glucose-induced vascular smooth muscle cell dysfunction via regulating ROCK1.

Abstract

MicroRNA-217 (miR-217) has been recently reported to be abnormally expressed during atherosclerosis. Nonetheless, it still remains unknown whether miR-217 can regulate inflammation, proliferation, migration, and apoptosis of vascular smooth muscle cells (VSMCs) in high-glucose condition. Sprague Dawley rats were used for establishing diabetic animal models. miR-217 mimics and miR-217 inhibitors were transfected into VSMCs. The miR-217 and ROCK1 expressions were measured by quantitative reverse transcription-polymerase chain reaction and Western blot. VSMCs' proliferation, migration, cell cycle, and apoptosis were validated using the Cell Counting Kit-8 assay, Transwell assay, and flow cytometry analysis, respectively. The binding sites between miR-217 and the 3'-untranslated region of ROCK1 were predicted via miRanda, PicTar, TargetScan, and microT databases, and the targeting relationship was confirmed by dual-luciferase reporter experiments. miR-217 was found to be upregulated in VSMCs treated by high glucose and aorta VSMCs of diabetic rats. Transfection of miR-217 mimics significantly induced VSMCs cycle arrest, inhibition of proliferation, reduction of migration, and enhancement of apoptosis. The bioinformatics analysis and dual-luciferase reporter experiments identified ROCK1 as a direct target of miR-217. miR-217 inhibits excessive proliferation and migration of VSMCs induced by high glucose by targeting ROCK1.