miR-141-3p Reduces Cell Migration and Proliferation in an In Vitro Modelof Atherosclerosis by Targeting Wnt5a

Background Atherosclerosis (AS) is a type of chronic vascular disease that is also a leading cause of numerous cardiovascular diseases in humans. The biomolecules responsible for the roles of microRNA (miR)-141-3p during AS development are less understood. Methods The relation between Wnt5a and miR-141-3p was predicted using bioinformatics software TargetScan 7.1, and confirmed via dual luciferase reporter assay. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and immunoblotting were conducted for examining miR-141-3p and Wingless and Int-1 (Wnt)5a expression levels. Additionally, transwell migration and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays were conducted for analyzing cell migration and proliferation, respectively. Results miR-141-3p was decreased in oxidized low-density lipoprotein (ox-LDL)-treated human vascular smooth muscle cells (VSMCs). Pretreatment with miR-141-3p mimic inhibited cell migration and proliferation in ox-LDL-induced VSMCs. Wnt5a was verified to act as the target of miR-141-3p in VSMCs. pcDNA3-Wnt5a partially reversed the effects of miR-141-3p mimic in ox-LDL-stimulated VSMCs. Conclusion miR-141-3p mimic decreased the damage in an AS model by targeting Wnt5a, thereby presenting a novel potential therapeutic target for treating AS.

Automated summary

miR-141-3p mimic reduced damage in an AS model by targeting Wnt5a, showing a potential novel therapeutic target for treating AS.