Lin Huang1, Ying Ding1, Lu Yang1, Xinghua Jiang1, Zhen Xia1, Zhigang You2. 1. Department of Cardiovascular Medicine, The Second Affiliated Hospital of NanChang University, Nanchang 330006, Jiangxi Province, China. 2. Department of Cardiovascular Medicine, The Second Affiliated Hospital of NanChang University, Nanchang 330006, Jiangxi Province, China. Electronic address: youzhigangznh@163.com.
Abstract
PURPOSE: To explore the role of SNHG16 in coronary heart disease (CHD) and its effect on vascular smooth muscle cells via miR-218-5p. METHODS: A quantitative real time polymerase chain reaction (qRT-PCR) assay was carried out to determine the expression of serum SNHG16 and miR-218-5p in the observation group before and after treatment and in the control group. Then, receiver operating characteristic (ROC) curves were drawn to analyze the value of SNHG16 and miR-218-5p in the diagnosis and prognosis prediction of CHD. Furthermore, purchased coronary artery smooth muscle cells (HCASMC) were transfected with SNHG16 mimics, SNHG16 inhibitor, miR-218-5p mimics, miR-218-5p inhibitor, or negative control, and then the cell proliferation, migration, apoptosis, and apoptosis-related proteins (Bax, Bcl-2, and Caspase-3) and Wnt/β-catenin signaling pathway-related proteins (c-myc and β-catenin) in the cells were detected. RESULTS: Both SNHG16 and miR-218-5 had good predictive value for the development and recurrence of CHD (P < 0.001). In addition, cell experiments showed that inhibition of SNHG16 weakened the proliferation and migration of HCASMC cells and intensified their apoptosis, SNHG16 and miR-218-5p had the same binding sites, and the dual luciferase reporter assay revealed that the fluorescence activity of HG16-WT was inhibited by transfected miR-mimics, but enhanced by transfected miR-inhibitor (both P < 0.050). Furthermore, the rescue experiment revealed that the effect of inhibiting SNHG16 on HCASMC cells was completely reversed by miR-218-5p (P > 0.050). CONCLUSIONS: Highly expressed SNHG16 targetedly regulates miR-218-5p and promotes the proliferation and migration of HCASMC via the Wnt/β-catenin signaling pathway, giving rise to CHD.
PURPOSE: To explore the role of SNHG16 in coronary heart disease (CHD) and its effect on vascular smooth muscle cells via miR-218-5p. METHODS: A quantitative real time polymerase chain reaction (qRT-PCR) assay was carried out to determine the expression of serum SNHG16 and miR-218-5p in the observation group before and after treatment and in the control group. Then, receiver operating characteristic (ROC) curves were drawn to analyze the value of SNHG16 and miR-218-5p in the diagnosis and prognosis prediction of CHD. Furthermore, purchased coronary artery smooth muscle cells (HCASMC) were transfected with SNHG16 mimics, SNHG16 inhibitor, miR-218-5p mimics, miR-218-5p inhibitor, or negative control, and then the cell proliferation, migration, apoptosis, and apoptosis-related proteins (Bax, Bcl-2, and Caspase-3) and Wnt/β-catenin signaling pathway-related proteins (c-myc and β-catenin) in the cells were detected. RESULTS: Both SNHG16 and miR-218-5 had good predictive value for the development and recurrence of CHD (P < 0.001). In addition, cell experiments showed that inhibition of SNHG16 weakened the proliferation and migration of HCASMC cells and intensified their apoptosis, SNHG16 and miR-218-5p had the same binding sites, and the dual luciferase reporter assay revealed that the fluorescence activity of HG16-WT was inhibited by transfected miR-mimics, but enhanced by transfected miR-inhibitor (both P < 0.050). Furthermore, the rescue experiment revealed that the effect of inhibiting SNHG16 on HCASMC cells was completely reversed by miR-218-5p (P > 0.050). CONCLUSIONS: Highly expressed SNHG16 targetedly regulates miR-218-5p and promotes the proliferation and migration of HCASMC via the Wnt/β-catenin signaling pathway, giving rise to CHD.