miR-185 silencing promotes the progression of atherosclerosis via targeting stromal interaction molecule 1

Abstract

Background: Atherosclerosis (AS) is a major risk factor for cardiovascular disease. microRNAs play a key role in gene regulation in the formation and development of atherosclerotic plaques. Herein, the role and target gene of miR-185 in AS were explored. Materials and methods: Cell viability, migration and invasion were examined by cell counting kit-8 (CCK-8) and transwell assay. The relative luciferase activity was measured by luciferase reporter assay. The levels of miR-185, STIM1, vascular endothelial growth factor (VEGF) and matrix metalloprotein-9 (MMP-9) were evaluated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot. Results: The results revealed that ox-LDL decreased miR-185 expression, and enhanced STIM1 expression in MOVAS cells, as well promoted cell viability, migration and invasion. 3ʹ-UTR of STIM1 contained miR-185 binding site according to the Targetscan. miR-185 silencing or STIM1 overexpression promoted the viability, migration and invasion of ox-LDL-induced MOVAS cells. miR-185 overexpression or STIM1 silencing had the opposite effect. Besides, miR-185 silencing upregulated the levels of VEGF and MMP-9 in vitro, and increased the lesions of arterial wall tissues and STIM1 positive rate in vivo. However, STIM1 silencing reversed these effects. Conclusions: Sum up, STIM1 was a potential target gene of miR-185 in AS. Knockdown of miR-185 facilitated the progression of AS through enhancing cell proliferation, migration and invasion via targeting STIM1. The research provides a novel view of miR-185/STIM1 axis function in AS development, and this targeting method may prevent and treat AS.

MicroRNA‑1323 serves as a biomarker in gestational diabetes mellitus and aggravates high glucose‑induced inhibition of trophoblast cell viability by suppressing TP53INP1

“…In recent years, microRNAs (miRNAs) have been recognized as important molecules in biological processes and are associated with various human diseases ( 22 ). For example, Fang et al ( 23 ) reported that miR-185 promoted the progression of atherosclerosis by targeting STIM1. A study by Liu et al ( 24 ) demonstrated that miR-34a promoted renal fibrosis by downregulating Klotho in tubular epithelial cells.…”

2,3,7,8‐Tetrachlorodibenzo‐p‐dioxin (TCDD) and Polychlorinated Biphenyl Coexposure Alters the Expression Profile of MicroRNAs in the Liver Associated with Atherosclerosis

“…The mechanism of TCDD-and PCB-induced atherosclerosis has been well characterized by many studies [21,23,39,40]. Emerging data continue to demonstrate the participation of miRNAs in atherosclerosis [41][42][43] and in biological responses induced by environmental pollutants [44][45][46]. However, there have been no previous reports on miRNA expression in TCDD-and PCB-induced atherosclerosis.…”

Long non-coding RNA MIAT regulates ox-LDL-induced cell proliferation, migration and invasion by miR-641/STIM1 axis in human vascular smooth muscle cells

“…And ectopic STIM1 expression impaired miR-641-mdiated effects on cell proliferation and metastasis in ox-LDL-stimulated VSMCs. The evidences from our research implicated STIM1 served as a promoter in the progression of ox-LDL-stimulated VSMCs, which was proved by the existed evidences [ 43 , 44 ]. In the meantime, the above data implied that miR-641 repressed the progression of VSMCs stimulated by ox-LDL via binding to STIM1.…”