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Hypoxia induces autophagy in cardiomyocytes via a hypoxia‑inducible factor 1‑dependent mechanism

  • Authors:
    • Lan Gui
    • Batu Liu
    • Guang Lv
  • View Affiliations / Copyright

    Affiliations: Department of Basic Theory, Sports Institute of Inner Mongolia University for the Nationalities, Tongliao, Inner Mongolia 028041, P.R. China, Sports Department, Sports Institute of Inner Mongolia University for the Nationalities, Tongliao, Inner Mongolia 028041, P.R. China, Institute of Pathogenic Microbiology and Immunology, Inner Mongolia University for the Nationalities, Tongliao, Inner Mongolia 028041, P.R. China
    Copyright: © Gui et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2233-2239
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    Published online on: March 24, 2016
       https://doi.org/10.3892/etm.2016.3190
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Abstract

Hypoxia frequently accompanies such vascular disorders as atherosclerosis, thrombosis and ischemia/reperfusion injury. Myocardial ischemia/reperfusion, in particular, is a major contributor to cardiomyocyte impairment. Autophagy is a dynamic, self‑catabolic process that has been implicated in a wide range of physiological processes and the pathogenesis of diverse diseases. The aim of the present study was to investigate the promotion of autophagy by hypoxia in a rat H9c2 heart cell line and determine the regulatory role of hypoxia‑inducible factor 1 (HIF‑1) in the hypoxia‑induced autophagy in H9c2 cells, using quantitative green fluorescent protein‑microtubule‑associated protein 1 light chain 3 analysis and electron microscopy of autophagic vesicles. In addition, western blot and quantitative polymerase chain reaction analysis of autophagy‑associated markers was conducted. In addition, the role of HIF‑1‑mediated autophagy in the hypoxia‑induced impairment of H9c2 cells was examined, as a measure of cellular viability, using an MTT assay. The results demonstrated that autophagy was induced in H9c2 cells under hypoxia, and the autophagy induction triggered by hypoxia could be enhanced by HIF‑1α overexpression and inhibited by HIF‑1α knockdown. Furthermore, the HIF‑1‑mediated autophagy ameliorated the reduction in the H9c2 cell viability induced by hypoxia. These findings provide a novel insight into the hypoxic‑ischemic injury to cardiomyocytes and give evidence for the occurrence of HIF‑1‑mediated autophagy in myocardial ischemia.
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Copy and paste a formatted citation
Spandidos Publications style
Gui L, Liu B and Lv G: Hypoxia induces autophagy in cardiomyocytes via a hypoxia‑inducible factor 1‑dependent mechanism. Exp Ther Med 11: 2233-2239, 2016.
APA
Gui, L., Liu, B., & Lv, G. (2016). Hypoxia induces autophagy in cardiomyocytes via a hypoxia‑inducible factor 1‑dependent mechanism. Experimental and Therapeutic Medicine, 11, 2233-2239. https://doi.org/10.3892/etm.2016.3190
MLA
Gui, L., Liu, B., Lv, G."Hypoxia induces autophagy in cardiomyocytes via a hypoxia‑inducible factor 1‑dependent mechanism". Experimental and Therapeutic Medicine 11.6 (2016): 2233-2239.
Chicago
Gui, L., Liu, B., Lv, G."Hypoxia induces autophagy in cardiomyocytes via a hypoxia‑inducible factor 1‑dependent mechanism". Experimental and Therapeutic Medicine 11, no. 6 (2016): 2233-2239. https://doi.org/10.3892/etm.2016.3190
Copy and paste a formatted citation
x
Spandidos Publications style
Gui L, Liu B and Lv G: Hypoxia induces autophagy in cardiomyocytes via a hypoxia‑inducible factor 1‑dependent mechanism. Exp Ther Med 11: 2233-2239, 2016.
APA
Gui, L., Liu, B., & Lv, G. (2016). Hypoxia induces autophagy in cardiomyocytes via a hypoxia‑inducible factor 1‑dependent mechanism. Experimental and Therapeutic Medicine, 11, 2233-2239. https://doi.org/10.3892/etm.2016.3190
MLA
Gui, L., Liu, B., Lv, G."Hypoxia induces autophagy in cardiomyocytes via a hypoxia‑inducible factor 1‑dependent mechanism". Experimental and Therapeutic Medicine 11.6 (2016): 2233-2239.
Chicago
Gui, L., Liu, B., Lv, G."Hypoxia induces autophagy in cardiomyocytes via a hypoxia‑inducible factor 1‑dependent mechanism". Experimental and Therapeutic Medicine 11, no. 6 (2016): 2233-2239. https://doi.org/10.3892/etm.2016.3190
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