Involvement of DJ‑1 in ischemic preconditioning‑induced delayed cardioprotection in vivo

  • Authors:
    • Huan Wang
    • Yuan‑Yuan Li
    • Ling‑Yu Qiu
    • Yu‑Feng Yan
    • Zhang‑Ping Liao
    • He‑Ping Chen
  • View Affiliations

  • Published online on: December 29, 2016     https://doi.org/10.3892/mmr.2016.6091
  • Pages: 995-1001
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

DJ‑1 protein, as a multifunctional intracellular protein, has been demonstrated to serve a critical role in regulating cell survival and oxidative stress. To provide in vivo evidence that DJ‑1 is involved in the delayed cardioprotection induced by ischemic preconditioning (IPC) against oxidative stress caused by ischemia/reperfusion (I/R), the present study subjected male Sprague‑Dawley rats to IPC (3 cycles of 5‑min coronary occlusion/5‑min reperfusion) 24 h prior to I/R (30‑min coronary occlusion/120‑min reperfusion). A lentiviral vector containing short hairpin RNA was injected into the left ventricle three weeks prior to IPC, to knockdown DJ‑1 in situ. Lactate dehydrogenase (LDH) and creatine kinase‑MB (CK‑MB) release, infarct size, cardiac function, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities, malondialdehyde (MDA), intracellular reactive oxygen species (ROS), and DJ‑1 protein expression levels were assessed. IPC caused a significant increase in the expression levels of DJ‑1 protein. In addition, IPC reduced LDH and CK‑MB release, attenuated myocardial infarct size, improved cardiac function following I/R, and inhibited the elevation of ROS and MDA and the decrease in activities of the antioxidant enzymes SOD, CAT and GPx. However, in situ knockdown of DJ‑1 attenuated the IPC‑induced delayed cardioprotection, and reversed the inhibitory effect of IPC on I/R‑induced oxidative stress. The present study therefore provided novel evidence that DJ‑1 is involved in the delayed cardioprotection of IPC against I/R injury in vivo. Notably, DJ‑1 is required for IPC to inhibit I/R‑induced oxidative stress.
View Figures
View References

Related Articles

Journal Cover

February-2017
Volume 15 Issue 2

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Wang H, Li YY, Qiu LY, Yan YF, Liao ZP and Chen HP: Involvement of DJ‑1 in ischemic preconditioning‑induced delayed cardioprotection in vivo. Mol Med Rep 15: 995-1001, 2017
APA
Wang, H., Li, Y., Qiu, L., Yan, Y., Liao, Z., & Chen, H. (2017). Involvement of DJ‑1 in ischemic preconditioning‑induced delayed cardioprotection in vivo. Molecular Medicine Reports, 15, 995-1001. https://doi.org/10.3892/mmr.2016.6091
MLA
Wang, H., Li, Y., Qiu, L., Yan, Y., Liao, Z., Chen, H."Involvement of DJ‑1 in ischemic preconditioning‑induced delayed cardioprotection in vivo". Molecular Medicine Reports 15.2 (2017): 995-1001.
Chicago
Wang, H., Li, Y., Qiu, L., Yan, Y., Liao, Z., Chen, H."Involvement of DJ‑1 in ischemic preconditioning‑induced delayed cardioprotection in vivo". Molecular Medicine Reports 15, no. 2 (2017): 995-1001. https://doi.org/10.3892/mmr.2016.6091