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CPNE3 interaction with RACK1 protects against myocardial ischemia/reperfusion injury

  • Authors:
    • Xiaoqun Zhang
    • Xue Han
    • Yanan Zhang
  • View Affiliations / Copyright

    Affiliations: Cardiology Department One, Cangzhou Central Hospital, Cangzhou, Hebei 061001, P.R. China
    Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 128
    |
    Published online on: December 10, 2021
       https://doi.org/10.3892/etm.2021.11051
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Abstract

Copine 3 (CPNE3) and receptor for activated C kinase 1 (RACK1) have been determined to be risk factors for patients with acute myocardial ischemia/reperfusion (I/R). The present study aimed to evaluate the role of CPNE3 and its interaction with RACK1 in myocardial (I/R) injury. Reverse transcription‑quantitative PCR (RT‑qPCR) and western blotting were performed to detect CPNE3 and RACK1 expression levels in H9c2 cells before and after the transfection of CPNE3 overexpression plasmid or small interfering RNA‑RACK1. Cell viability was detected using a Cell Counting Kit‑8 assay, and immunoprecipitation assays were performed to determine the interaction between CPNE3 and RACK1. A commercial kit was used to examine lactate dehydrogenase (LDH) levels. The expression levels of inflammatory cytokines were detected via RT‑qPCR and western blotting. Cell apoptosis was assessed via TUNEL staining and western blotting. The results demonstrated that the expression levels of CPNE3 and RACK1 were decreased in hypoxia/reoxygenation (H/R)‑induced H9c2 cardiomyocytes, which was consistent with the expression levels observed in the myocardial I/R injury rat model. It was found that CPNE3 overexpression upregulated RACK1 expression, increased cell viability and suppressed the release of LDH in H/R‑induced H9c2 cells. Furthermore, CPNE3 overexpression inhibited the release of inflammatory cytokines and decreased cell apoptosis in H/R‑induced cardiomyocytes by activating RACK1 expression. The present study suggested that CPNE3 served an important role in preventing I/R injury by interacting with RACK1, providing novel insight into the prevention of myocardial I/R injury, as well as the treatment and care of patients with myocardial I/R.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang X, Han X and Zhang Y: CPNE3 interaction with RACK1 protects against myocardial ischemia/reperfusion injury. Exp Ther Med 23: 128, 2022.
APA
Zhang, X., Han, X., & Zhang, Y. (2022). CPNE3 interaction with RACK1 protects against myocardial ischemia/reperfusion injury. Experimental and Therapeutic Medicine, 23, 128. https://doi.org/10.3892/etm.2021.11051
MLA
Zhang, X., Han, X., Zhang, Y."CPNE3 interaction with RACK1 protects against myocardial ischemia/reperfusion injury". Experimental and Therapeutic Medicine 23.2 (2022): 128.
Chicago
Zhang, X., Han, X., Zhang, Y."CPNE3 interaction with RACK1 protects against myocardial ischemia/reperfusion injury". Experimental and Therapeutic Medicine 23, no. 2 (2022): 128. https://doi.org/10.3892/etm.2021.11051
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang X, Han X and Zhang Y: CPNE3 interaction with RACK1 protects against myocardial ischemia/reperfusion injury. Exp Ther Med 23: 128, 2022.
APA
Zhang, X., Han, X., & Zhang, Y. (2022). CPNE3 interaction with RACK1 protects against myocardial ischemia/reperfusion injury. Experimental and Therapeutic Medicine, 23, 128. https://doi.org/10.3892/etm.2021.11051
MLA
Zhang, X., Han, X., Zhang, Y."CPNE3 interaction with RACK1 protects against myocardial ischemia/reperfusion injury". Experimental and Therapeutic Medicine 23.2 (2022): 128.
Chicago
Zhang, X., Han, X., Zhang, Y."CPNE3 interaction with RACK1 protects against myocardial ischemia/reperfusion injury". Experimental and Therapeutic Medicine 23, no. 2 (2022): 128. https://doi.org/10.3892/etm.2021.11051
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