miR‑541‑3p inhibits the viability and migration of vascular smooth muscle cells via targeting STIM1.

The transformation of vascular smooth muscle cells (VSMCs) into the proliferative migratory phenotype in the plaque area contributes to stable plaque formation and facilitates the pathogenesis of atherosclerosis. Stromal interaction molecule 1 (STIM1) has been identified to promote the proliferation of VSMCs, suggesting that STIM1 may be a potent target for the prevention and treatment of atherosclerosis. Bioinformatics analysis has previously predicted STIM1 as a target of microRNA (miR)‑541‑3p. The present study aimed to determine the effect of the miR‑541‑3p/STIM1 axis on the progression of atherosclerosis . Oxidized low‑density lipoprotein (ox‑LDL)‑treated VSMCs were used as an atherosclerosis model. Cell Counting Kit‑8 and Transwell migration assays were used to analyze cell viability and migration, respectively. Reverse transcription‑quantitative PCR and western blotting were applied to measure mRNA and protein expression levels, respectively. The association between miR‑541‑3p and STIM1 was detected using a dual luciferase gene reporter assay. The results of the present study revealed that ox‑LDL treatment significantly downregulated miR‑541‑3p expression levels and upregulated STIM1 expression levels in VSMCs. In addition, ox‑LDL stimulation enhanced cell viability and migration. The overexpression of miR‑541‑3p significantly reversed the ox‑LDL‑mediated increase in cell viability and migration, whereas the knockdown of miR‑541‑3p expression enhanced the ox‑LDL‑mediated effects. STIM1 was confirmed to be a target gene of miR‑541‑3p in VSMCs. The knockdown of STIM1 significantly impaired the stimulatory effects of miR‑541‑3p knockdown on cell viability and migration. In conclusion, the findings of the present study suggested that miR‑541‑3p may efficiently repress VSMC viability and migration by targeting STIM1 under the treatment of ox‑LDL. These results indicated that the miR‑541‑3p/STIM1 axis may represent a potent target to modulate VSMC viability and migration.