title: MiR-206 Suppresses the Progression of Coronary Artery Disease by Modulating Vascular Endothelial Growth Factor (VEGF) Expression.
abstract: BACKGROUND We investigated whether microRNA-206 (miR-206) is abnormally expressed in patients with coronary artery disease (CAD). The potential mechanism by which miR-206 may regulate CAD progression was also studied. MATERIAL AND METHODS A total of 78 CAD patients in the case group and 65 subjects in the control group were enrolled in this study so that the correlation between miR-206 and CAD could be accurately determined. Serum total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides were detected using a biochemistry analyzer. MiR-206 and vascular endothelial growth factor (VEGF) expression levels were tested using either reverse transcription polymerase chain reaction or western blot. Associations between miR-206 expression and different clinicopathological features of CAD patients were also analyzed. CAD cells were transfected with miR-206 mimic (miR-206), its negative control (miR-NC), miR-206 inhibitor (anti-miR-206), and its negative control (anti-miR-NC), respectively. Flow cytometry was conducted to explore the function of miR-206 in CAD cell apoptosis after transfection. Moreover, transwell assay was carried out to study the migratory ability of endothelial progenitor cells (EPCs) in CAD patients. RESULTS MiR-206 expression was enriched in both diseased EPCs and plasma of CAD patients. No significant correlation was found between decrease in miR-206 expression and different clinicopathological features. In addition, miR-206 significantly suppressed the viability and invasion of EPCs in CAD patients, and it promoted the apoptosis of their EPCs. Moreover, we found that miR-206 is able to inhibit VEGF expression. CONCLUSIONS As suggested by our study, MiR-206 can be a novel benign biomarker for CAD because it may regulate VEGF expression.
authors.affiliation: Department of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China (mainland).
authors.forename: Maojing
authors.initials: M
authors.lastname: Wang
authors.affiliation: Department of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China (mainland).
authors.forename: Yang
authors.initials: Y
authors.lastname: Ji
authors.affiliation: Department of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China (mainland).
authors.forename: Shanglang
authors.initials: S
authors.lastname: Cai
authors.affiliation: Department of Ophthalmology, Huangdao District People's Hospital, Qingdao, Shandong, China (mainland).
authors.forename: Wei
authors.initials: W
authors.lastname: Ding
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D017209:Apoptosis / Q000235:genetics; D016022:Case-Control Studies; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation / Q000235:genetics; D002478:Cells, Cultured; D003324:Coronary Artery Disease / Q000097:blood / Q000235:genetics* / Q000473:pathology; D018450:Disease Progression; D015536:Down-Regulation; D066026:Endothelial Progenitor Cells / Q000473:pathology; D005260:Female; D006801:Humans; D008297:Male; D035683:MicroRNAs / Q000096:biosynthesis* / Q000235:genetics; D008875:Middle Aged; D014162:Transfection; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics
chemical_list: C546087:MIRN206 microRNA, human; D035683:MicroRNAs; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A