HIF‑1α may provide only short‑term protection against ischemia‑reperfusion injury in Sprague‑Dawley myocardial cultures

  • Authors:
    • Siyang Wang
    • Xin Shao
    • Xiaoxue Li
    • Xiaojuan Su
    • Yongxu Huo
    • Chunlei Yang
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  • Published online on: February 3, 2016     https://doi.org/10.3892/mco.2016.764
  • Pages: 579-583
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Abstract

Hypoxia‑inducible factor‑1 (HIF‑1α) exerts an important role in protecting against cardiac tissue damage, for example, following ischemia‑reperfusion (I/R), although the time frame during which it acts has yet to be fully elucidated. In the present study, a culture model of myocardial cells from Sprague‑Dawley rats was used to examine the expression levels of HIF‑1α and various downstream effectors at different times following I/R. The levels of HIF‑1α were manipulated by overexpressing HIF‑1α prior to I/R. HIF‑1α levels peaked at 6 h following I/R, subsequently decreasing to low levels. The levels of downstream effectors peaked at 48 h, and decreased almost to pre‑I/R levels by 72 h. These results suggest that HIF‑1α and its downstream targets offer only short‑term protection following I/R. These results may have implications for the treatment of I/R‑associated injury in a variety of clinical contexts.
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April 2016
Volume 4 Issue 4

Print ISSN: 2049-9450
Online ISSN:2049-9469

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APA
Wang, S., Shao, X., Li, X., Su, X., Huo, Y., & Yang, C. (2016). HIF‑1α may provide only short‑term protection against ischemia‑reperfusion injury in Sprague‑Dawley myocardial cultures. Molecular and Clinical Oncology, 4, 579-583. https://doi.org/10.3892/mco.2016.764
MLA
Wang, S., Shao, X., Li, X., Su, X., Huo, Y., Yang, C."HIF‑1α may provide only short‑term protection against ischemia‑reperfusion injury in Sprague‑Dawley myocardial cultures". Molecular and Clinical Oncology 4.4 (2016): 579-583.
Chicago
Wang, S., Shao, X., Li, X., Su, X., Huo, Y., Yang, C."HIF‑1α may provide only short‑term protection against ischemia‑reperfusion injury in Sprague‑Dawley myocardial cultures". Molecular and Clinical Oncology 4, no. 4 (2016): 579-583. https://doi.org/10.3892/mco.2016.764