Open Access

Protective effect of angiotensin-(1-7) against hyperglycaemia-induced injury in H9c2 cardiomyoblast cells via the PI3K̸Akt signaling pathway

Corrigendum in: /10.3892/ijmm.2017.3322

  • Authors:
    • Yi-Ying Yang
    • Xiu-Ting Sun
    • Zheng-Xun Li
    • Wei-Yan Chen
    • Xiang Wang
    • Mei-Ling Liang
    • Hui Shi
    • Zhi-Sheng Yang
    • Wu-Tao Zeng
  • View Affiliations

  • Published online on: December 15, 2017     https://doi.org/10.3892/ijmm.2017.3322
  • Pages: 1283-1292
  • Copyright : © Yang et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].

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Abstract

Angiotensin-(1-7) [Ang-(1-7)], a heptapeptide mainly generated from cleavage of AngⅠ and AngⅡ, possesses physiological and pharmacological properties, including anti‑inflammatory and antidiabetic properties. Activation of the phosphoinositide 3-kinase and protein kinase B (PI3K̸Akt) signaling pathway has been confirmed to participate in cardioprotection against hyperglycaemia-induced injury. The aim of the present study was to test the hypothesis that Ang-(1-7) protects H9c2 cardiomyoblast cells against high glucose (HG)-induced injury by activating the PI3K̸Akt pathway. To examine this hypothesis, H9c2 cells were treated with 35 mmol/l (mM) glucose (HG) for 24 h to establish a HG-induced cardiomyocyte injury model. The cells were co-treated with 1 µmol/l (µM) Ang-(1-7) and 35 mM glucose. The findings of the present study demonstrated that exposure of H9c2 cells to HG for 24 h markedly induced injury, as evidenced by an increase in the percentage of apoptotic cells, generation of reactive oxygen species and level of inflammatory cytokines, as well as a decline in cell viability and mitochondrial luminosity. These injuries were significantly attenuated by co-treatment of the cells with Ang-(1-7) and HG. In addition, PI3K̸Akt phosphorylation was suppressed by HG treatment, but this effect was abolished when the H9c2 cells were co-treated with Ang-(1-7) and HG. Furthermore, the cardioprotection of Ang-(1-7) against HG-induced injury in H9c2 cardiomyoblasts was highly attenuated in the presence of either D-Ala7-Ang-(1-7) (A-779, an antagonist of the Mas receptor) or LY294002 (an inhibitor of PI3K̸Akt). In conclusion, the present study provided new evidence that Ang-(1-7) protects H9c2 cardiomyoblasts against HG-induced injury by activating the PI3K̸Akt signaling pathway.
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March 2018
Volume 41 Issue 3

Print ISSN: 1107-3756
Online ISSN:1791-244X

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APA
Yang, Y., Sun, X., Li, Z., Chen, W., Wang, X., Liang, M. ... Zeng, W. (2018). Protective effect of angiotensin-(1-7) against hyperglycaemia-induced injury in H9c2 cardiomyoblast cells via the PI3K̸Akt signaling pathway Corrigendum in /10.3892/ijmm.2017.3322. International Journal of Molecular Medicine, 41, 1283-1292. https://doi.org/10.3892/ijmm.2017.3322
MLA
Yang, Y., Sun, X., Li, Z., Chen, W., Wang, X., Liang, M., Shi, H., Yang, Z., Zeng, W."Protective effect of angiotensin-(1-7) against hyperglycaemia-induced injury in H9c2 cardiomyoblast cells via the PI3K̸Akt signaling pathway Corrigendum in /10.3892/ijmm.2017.3322". International Journal of Molecular Medicine 41.3 (2018): 1283-1292.
Chicago
Yang, Y., Sun, X., Li, Z., Chen, W., Wang, X., Liang, M., Shi, H., Yang, Z., Zeng, W."Protective effect of angiotensin-(1-7) against hyperglycaemia-induced injury in H9c2 cardiomyoblast cells via the PI3K̸Akt signaling pathway Corrigendum in /10.3892/ijmm.2017.3322". International Journal of Molecular Medicine 41, no. 3 (2018): 1283-1292. https://doi.org/10.3892/ijmm.2017.3322