title: Cardioprotective effect of miR-214 in myocardial ischemic postconditioning by down-regulation of hypoxia inducible factor 1, alpha subunit inhibitor.
abstract: To determine the significance of miR&mdash;214 expression in ischemic post&mdash;conditioning. Sixty rats were grouped to establish animal models. Immuno&mdash; luminescence and chemical methods were used to detect oxidative stress indicators. Hemodynamics indexes were measured by carotid artery intubation, and ischemia and infarction areas by Evans blue and 2,3&mdash;5 triphenyltetrazolium chloride(TTC) staining. TargetScan was used for identification and luciferase assays for verification of target genes.miR&mdash;214 and hypoxia inducible factor 1, alpha subunit inhibitor (HIF1AN) were analyzed by real&mdash;time quantitative polymerase chain reaction. Ischemia reperfusion significantly decreased left ventricular systolic pressure, +dp/dtmax, and &mdash;dp/dtmax and increased left ventricular end&mdash;diastolic pressure; ischemic post&mdash;conditioning had contrasting effects. Compared to the sham group, the ischemic/reperfusion (IR) group showed increased creatine kinase isoenzyme (CK&mdash;MB) and malondialdehyde (MDA) in the myocardium and decreased SOD. miR&mdash;214 in the IR group was down&mdash;regulated, and HIF1AN, up&mdash;regulated. Compared with the IR group, the ischemia postconditioning (IPC) group showed decreased CK&mdash;MB and MDA in the myocardium and increased SOD. The proportion of infarction area to ischemia area in IPC group declined compared to IR group. miR&mdash;214 and HIF1AN in the IPC group showed significant up&mdash; and down&mdash;regulation, respectively. Ischemic postconditioning can improve myocardial function, reduce myocardial infarction area, and prevent the ischemia reperfusion injury. miR&mdash;214 may participate in the protective function of ischemic post&mdash;conditioning by down&mdash;regulating HIF1AN.
authors.affiliation: Zhengzhou People&apos;s Hospital Department of Cardiology Zhengzhou China.
authors.forename: D-Y
authors.initials: DY
authors.lastname: Wan
authors.affiliation: Zhengzhou People&apos;s Hospital Department of Cardiology Zhengzhou China.
authors.forename: Z
authors.initials: Z
authors.lastname: Zhang
authors.affiliation: Henan Provincial People&apos;s Hospital Department of Cardiology Zhengzhou China honghyang&commat;163.com.
authors.forename: H-H
authors.initials: HH
authors.lastname: Yang
mesh_terms: D000818:Animals; D002316:Cardiotonic Agents / Q000378:metabolism*; D002339:Carotid Arteries / Q000473:pathology; D052279:Creatine Kinase, MB Form / Q000097:blood; D015536:Down-Regulation; D006439:Hemodynamics / Q000502:physiology; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000037:antagonists & inhibitors / Q000235:genetics; D057775:Ischemic Postconditioning; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D006899:Mixed Function Oxygenases / Q000235:genetics / Q000378:metabolism*; D009203:Myocardial Infarction / Q000473:pathology; D017202:Myocardial Ischemia / Q000473:pathology*; D009206:Myocardium / Q000473:pathology; D018384:Oxidative Stress / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury; D013482:Superoxide Dismutase / Q000097:blood; D017725:Ventricular Pressure / Q000502:physiology
chemical_list: D002316:Cardiotonic Agents; C497444:Hif1a protein, rat; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D035683:MicroRNAs; C559947:Mirn214 microRNA, rat; D008315:Malondialdehyde; D006899:Mixed Function Oxygenases; C000606147:HIF1AN protein, rat; D013482:Superoxide Dismutase; D052279:Creatine Kinase, MB Form