MiR‐217 alleviates high‐glucose‐induced vascular smooth muscle cell dysfunction via regulating ROCK1. Issue 3 (6th December 2020)

• Record Type: Journal Article
• Authors: Zhou, Wan; Ye, Shandong; Wang, Wei
• Is Part Of: Journal of biochemical and molecular toxicology. Volume 35:Issue 3(2021)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2020-12-06
• Subjects: atherosclerosis -- diabetes -- miR‐217 -- ROCK1 -- vascular smooth muscle cell; Biochemistry -- Periodicals; Molecular biology -- Periodicals; Toxicology -- Periodicals; 574
• DOI: 10.1002/jbt.22668
• Languages: English
• ISSNs: 1095-6670

Abstract

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.