06 October 2016 : Laboratory Research
Effects of mir-21 on Cardiac Microvascular Endothelial Cells After Acute Myocardial Infarction in Rats: Role of Phosphatase and Tensin Homolog (PTEN)/Vascular Endothelial Growth Factor (VEGF) Signal PathwayFeng YangB, Wenwei LiuBC, Xiaojuan YanDE, Hanyun ZhouBCF, Hongshen ZhangDE, Jianfei LiuBC, Ming YuDE, Xiaoshan ZhuCDF, Kezhong MaAEG
Med Sci Monit 2016; 22:3562-3575
BACKGROUND: This study investigated how miR-21 expression is reflected in acute myocardial infarction and explored the role of miR-21 and the PTEN/VEGF signaling pathway in cardiac microvascular endothelial cells.
MATERIAL AND METHODS: We used an in vivo LAD rat model to simulate acute myocardial infarction. MiR-21 mimics and miR-21 inhibitors were injected and transfected into model rats in order to alter miR-21 expression. Cardiac functions were evaluated using echocardiographic measurement, ELISA, and Masson staining. In addition, lenti-PTEN and VEGF siRNA were transfected into CMEC cells using standard procedures for assessing the effect of PTEN and VEGE on cell proliferation, apoptosis, and angiogenesis. MiR-21, PTEN, and VEGF expressions were examined by RT-PCR and Western blot. The relationship between miR-21 and PTEN was determined by the luciferase activity assay.
RESULTS: We demonstrated that miR-21 bonded with the 3’-UTR of PTEN and suppressed PTEN expressions. Established models significantly induced cardiac infarct volume and endothelial injury marker expressions as well as miR-21 and PTEN expressions (P<0.05). MiR-21 mimics exhibited significantly protective effects since they down-regulated both infarction size and injury marker expressions by increasing VEGF expression and inhibiting PTEN expression (P<0.05). In addition, results from in vitro research show that lenti-PTEN and VEGF siRNA can notably antagonize the effect of miR-21 on cell proliferation, apoptosis, and angiogenesis (P<0.05).
CONCLUSIONS: MiR-21 exerts protective effects on endothelial injury through the PTEN/VEGF pathway after acute myocardial infarction.
Keywords: Apoptosis - genetics, Angiogenesis Inhibitors - metabolism, 3' Untranslated Regions, Endothelial Cells - pathology, mesenchymal stromal cells, Microvessels - pathology, Myocardial Infarction - pathology, Neovascularization, Pathologic - pathology, PTEN Phosphohydrolase - metabolism, Signal Transduction, Tensins - metabolism, Vascular Endothelial Growth Factor A - metabolism
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