Upregulation of FoxM1 protects against ischemia/reperfusion-induced myocardial injury

  • Gang Zhang Department of Cardiology, The Affiliated Huaian No.1 People’s Hospital of Nanjing Medical University, Huai ‘an, Jiangsu Province, 223300, China;
  • Kun Yu Department of Cardiology, The Affiliated Huaian No.1 People’s Hospital of Nanjing Medical University, Huai ‘an, Jiangsu Province, 223300, China;
  • Zhi Bao Department of Cardiology, The Affiliated Huaian No.1 People’s Hospital of Nanjing Medical University, Huai ‘an, Jiangsu Province, 223300, China;
  • Xiaofeng Sun Department of Pediatric, The Affiliated Huaian No.1 People’s Hospital of Nanjing Medical University, Huai ‘an, Jiangsu Province, 223300, China
  • Dongying Zhang Department of Cardiology, The Affiliated Huaian No.1 People’s Hospital of Nanjing Medical University, Huai ‘an, Jiangsu Province, 223300, China;
DOI: https://doi.org/10.18388/abp.2020_5536

Abstract

Background. Ischemia/reperfusion (I/R) induced lethal tissue injury in myocardium. FoxM1 (Forkhead Box M1), expressed in proliferating cardiac progenitor cells, could regulate myocardial development. However, the role of FoxM1 in I/R-induced myocardial injury has not been reported yet. Methods. Rats were conducted with regional ischemia followed by reperfusion in myocardium through ligation of the left anterior descending coronary artery. Triphenyl-tetrazolium chloride staining was utilized to assess the infarct size. ELISA was performed to detect activities of creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH). Protein expression of FoxM1 in heart tissues and H9c2 were determined by western blot. H9c2 cells were used to establish a hypoxia/reoxygenation cell model, and the cell viability, proliferation and apoptosis were evaluated by MTT, EdU (5-ethynyl-2’-deoxyuridine) staining and TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) staining, respectively. Adenovirus (Ad)-mediated over-expression of FoxM1 was injected into the anterior wall of the left ventricle of rats to evaluate the role of FoxM1 on in vivo I/R-induced myocardial injury. Results. FoxM1 was reduced in heart tissues isolated from rats post myocardial I/R injury. Forced FoxM1 expression increased cell viability and proliferation of hypoxia/reoxygenation-induced H9c2, while repressed the cell apoptosis with increased Bcl-2 and decreased Bax and cleaved caspase-3. Injection of Ad-FoxM1 suppressed infarct size of the heart and decreased activities of CK-MB and LDH. Conclusion. FoxM1 attenuated I/R-induced myocardial injury, providing potential therapeutic target for the disease.

Published
2021-08-17
Issue
Vol. 68 No. 4 (2021)
Section
Articles

Copyright (c) 2021 Gang Zhang, Kun Yu, Zhi Bao, Xiaofeng Sun, Dongying Zhang

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