Abstract
BACKGROUND: Increasing evidence showed that lncRNAs are involved in the procession of atherosclerosis (AS). This study detected MAGI2-AS3 expression in the serum of AS patients and further investigated the mechanism of MAGI2-AS3 in AS. METHODS: MAGI2-AS3 and miR-525-5p in the AS patients' serum and oxidized low-density lipoprotein (ox-LDL) induced human coronary artery smooth muscle cells (HCASMCs) were quantified by qRT-PCR. Spearman correlation was calculated between MAGI2-AS3 and clinical indexes or miR-525-5p. ROC curve analyzed the clinical diagnostic performance of MAGI2-AS3. Small interfering RNA targeting MAGI2-AS3 (si-MAGI2-AS3) silenced MAGI2-AS3 expression. HCASMCs proliferation, migration, and apoptosis were assayed by CCK-8, transwell, and flow cytometry, respectively. The target miR-525-5p was predicted by StarBase and verified by dual-luciferase reporter assay and co-transfection. RESULTS: MAGI2-AS3 increased in the AS patients' serum and ox-LDL-induced HCASMCs. MAGI2-AS3 was negatively associated with C-reactive protein (CRP) and carotid intima-media thickness (CIMT). The ROC curve confirmed the efficacy of MAGI2-AS3 in distinguishing AS from control subjects. Silencing MAGI2-AS3 reversed the enhancement of proliferation and migration and the reduction of apoptosis caused by ox-LDL in HCASMCs. MiR-525-5p was predicted as a target and further verified by dual-luciferase assay. MiR-525-5p declined in both the serum of AS patients and ox-LDL-induced HCASMCs. Rescue experiments showed that miR-525-5p downregulation inverted the decrease in proliferation and migration, and the increase in apoptosis due to si-MAGI2-AS3 treatment. CONCLUSIONS: In summary, our study demonstrated that MAGI2-AS3 participates in AS progression by sponging the miR-525-5p, indicating that MAGI2-AS3 may be a potential biomarker of AS.