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To investigate the role of small nucleolus RNA host gene 14 (SNHG14) in the progression of atherosclerosis (AS), bioinformatics analysis, and other relevant experiments (cell counting kit-8, flow cytometry, quantitative real-time polymerase chain reaction, luciferase reporter, RNA immunoprecipitation, RNA pull-down, and western blot assays) were done. The current study revealed that SNHG14 level was high in the serum of AS patients and oxidized low-density lipoprotein (ox-LDL)-induced AS cell lines. Besides, we found that SNHG14 accelerated cell proliferation while inhibited cell apoptosis in ox-LDL-induced AS cell lines. Next, SNHG14 was confirmed to be a sponge for miR-186-5p in AS cells, and it was validated that SNHG14 regulated AS cell proliferation and apoptosis by sponging miR-186-5p. Moreover, we uncovered that WAS-interacting protein family member 2 (WIPF2) was a downstream target of miR-186-5p in AS cells. Finally, it was demonstrated that miR-186-5p modulated AS cell proliferation and apoptosis via targeting WIPF2. To conclude, our research disclosed that SNHG14 affected ox-LDL-induced AS cell proliferation and apoptosis through miR-186-5p/WIPF2 axis, which may provide a theoretical basis for the treatment and diagnosis of AS.

Background. The expression of the platelet-derived growth factor (PDGF), angiopoietin-1 (Ang-1) in patients with coronary artery disease of different studies was inconsistent. This study was to investigate the expression of the PDGF and Ang-1 in peripheral blood and coronary artery in patients with acute coronary syndrome (ACS) and the relationship between the expression of the PDGF and Ang-1 and the severity of coronary artery disease. Methods. A total of 81 patients with acute coronary syndrome undergoing coronary angiography were enrolled from September 2012 to December 2013. Patients with ACS included 61 patients with acute myocardial infarction (AMI group) and 20 patients with unstable angina pectoris (UAP group). The 29 patients who were hospitalized for chest pain undergoing coronary angiography without stenosis and with TIMI level 3 blood flow were selected as the control group. During coronary arteriography (CAG) or percutaneous coronary intervention (PCI), blood in the peripheral artery and in the local coronary artery was collected from all the patients. Serum PDGF and Ang-1 levels were measured by ELISA. We calculated the Gensini score of each patient with CHD according to the result of CAG. Patients with ACS were followed up, and the major adverse cardiovascular and cerebrovascular adverse events were recorded. Results. In peripheral blood, the concentration of the PDGF was significantly elevated in the ACS group than that of the control group. The level of the PDGF in the AMI group was significantly higher than that in the UAP group. In coronary artery blood, the level of the PDGF in the ACS group was significantly higher than that of the UAP group. There was no significant difference in the concentration of Ang-1 in peripheral blood between patients with coronary heart disease and the control group. The concentration of Ang-1 in the coronary artery was significantly lower than that in peripheral blood. The coronary Ang-1 concentrations in the ACS group were significantly higher than those in the UAP group. The concentrations of the PDGF and Ang-1 in peripheral and coronary artery blood were positively correlated with the severity of coronary lesions. Patients with MACCE had higher PDGF and Ang-1 levels in the coronary sinus. Conclusion. The serum PDGF concentration in patients with acute coronary syndrome was significantly increased, especially in the local coronary artery. The serum Ang-1 in the coronary artery was significantly increased in patients with acute myocardial infarction and was related to the degree of coronary artery stenosis. Coronary sinus PDGF and Ang-1 levels can reflect the severity of lesions in patients with acute coronary syndrome.