MiR-25 exerts cardioprotective effect in a rat model of myocardial ischemia-reperfusion injury by targeting high-mobility group box 1. Issue 1 (January 2020)

• Record Type: Journal Article
• Authors: Liu, Qifang; Song, Bo; Xu, Min; An, Yaping; Zhao, Yidong; Yue, Feng
• Is Part Of: Journal of the Chinese Medical Association. Volume 83:Issue 1(2020)
• Publication Date: 2020-01
• Subjects: Animal experiment -- Ischemia-reperfusion injury -- Myocardium; Medicine -- Periodicals; 610.5
• DOI: 10.1097/JCMA.0000000000000229
• Languages: English
• ISSNs: 1726-4901

Abstract

Abstract : Background: We previously confirmed the targeting of high-mobility group box 1 (HMGB1) by miR-25. This project aims to further investigate whether miR-25 improves myocardial ischemia-reperfusion injury (IRI) in vivo by targeting HMGB1. Methods: A rat model of myocardial IRI was established by the ligation of the left anterior descending coronary artery for 45 minutes followed by 2, 4, or 6 hours reperfusion. The expression of miR-25, HMGB1, and apoptosis-related proteins in the myocardium was determined by quantitative real-time polymerase chain reaction (PCR) and western blotting. The activities of myocardial enzymes and the release of inflammatory cytokines were evaluated by enzyme-linked immunosorbent assay. Evans blue/triphenyltetrazolium chloride double staining was performed to assess infarct size. Myocardial apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Results: MiR-25 expression was significantly downregulated, while HMGB1 was highly expressed at the mRNA and protein levels in myocardial tissues after induction of the IRI model. MiR-25 agomir administration suppressed the expression of HMGB1 in myocardial tissues. Furthermore, administration of both miR-25 agomir and lentivirus-mediated short hairpin RNA (shRNA) interference targeting HMGB1 sh-HMGB1 resulted in reduced serum myocardial enzyme activities, cytokine secretion, and myocardial apoptosis during myocardial IRI. Conclusion: MiR-25 mitigated myocardial IRI-induced damage by targeting HMGB1.