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Original Research

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

ORCID Icon, &
Pages 598-604 | Published online: 05 Apr 2021
 

Abstract

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.

Disclosure statement

No potential competing interest was reported by the author(s).

Author contributions

FZ designed the experiments, analyzed the data, and prepared the manuscript. PS and NY carried out the experiments and analyzed the data.

Data availability statement

The data and materials that support the results or analyses presented in our paper are not available, because they are related with another project.

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