Klotho overexpression suppresses apoptosis by regulating the Hsp70/Akt/Bad pathway in H9c2(2-1) cells
- Jinpeng Hu
- Bin Su
- Xuewen Li
- Yuming Li
- Jihong Zhao
Affiliations: Graduate School of Tianjin Medical University, Tianjin 300070, P.R. China, Ministry of Research, Characteristic Medical Center of The Chinese People's Armed Police Force, Tianjin 300162, P.R. China, Department of Geriatric Medicine, Characteristic Medical Center of Chinese People's Armed Police Force, Tianjin 300162, P.R. China, Angiocardiopathy Institute of Characteristic Medical Center of PAP, Tianjin 300162, P.R. China
- Published online on: March 16, 2021 https://doi.org/10.3892/etm.2021.9917
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Early reperfusion is the most effective and important treatment for acute myocardial infarction. However, reperfusion therapy often leads to a certain degree of myocardial damage. The aim of the present study was to identify the role of klotho, and the molecular mechanism underlying its effects, in myocardial damage using a model of myocardial hypoxia injury. Hypoxia/reoxygenation (H/R) was used to mimic ischemia/reperfusion (I/R) injury in vitro. The expression and distribution of klotho in H9c2(2‑1) cells was observed by fluorogenic scanning, and the apoptotic rate was determined by Annexin V‑FITC/propidium iodide dual staining. Cell viability was determined by MTT assay, and caspase‑3, cleaved caspase‑3, Bcl‑2, Bax, heat shock protein (Hsp) 70 and Akt levels were assessed by western blotting. A lactate dehydrogenase test was performed to determine the degree of H9c2(2‑1) cell damage. The results revealed that klotho was primarily located in the cytoplasm of H9c2(2‑1) cells. Klotho overexpression markedly suppressed H/R‑induced H9c2(2‑1) cell apoptosis. Furthermore, cell viability increased, and injury decreased in response to klotho. Klotho also suppressed the activation of caspase‑3, upregulated Bcl2 and decreased Bax levels following H/R injury, as well as alleviating H/R injury by upregulating the expression of Hsp70 and increasing the levels of phosphorylated (p‑)Akt and Bad. In conclusion, these results indicate that klotho suppressed H/R‑induced H9c2(2‑1) cell apoptosis by regulating the levels of Hsp70, p‑Akt and p‑Bad, which suggest that klotho could be a novel agent for the treatment of coronary disease.