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Med Sci Monit. 2014 Jun 19;20:1017-23. doi: 10.12659/MSM.890897.

Reactive oxygen species contribute to simulated ischemia/reperfusion-induced autophagic cell death in human umbilical vein endothelial cells.

Author information

1
Department of Cardiology, People's Hospital of Hainan Province, Haikou, China (mainland).

Abstract

BACKGROUND:

Autophagy is important for cells to degrade protein aggregates and organelles. Our preliminary study suggests that ischemia/reperfusion in rabbit hearts promoted autophagic myocardial injury, resulting in no-reflow phenomenon. In this study, we sought to further understand the mechanism and outcome of the upregulation of autophagy in ischemia/reperfusion.

MATERIAL AND METHODS:

We employed a simulated ischemia/reperfusion (sI/R) model in human umbilical vein endothelial cells (HUVECs) in vitro, in the presence or absence of antioxidants.

RESULTS:

Our study confirms that sI/R induces autophagy in HUVECs as measured by increased expression of Beclin 1 and microtubule-associated protein 1 light chain 3 (LC3), electron microscopic analysis, and special biofluorescent staining with monodansylcadaverine. This sI/R-induced autophagy was also accompanied by increased levels of p65 protein expression and cell death. In addition, we detected the accumulation of reactive oxygen species (ROS) after sI/R. Moreover, with the application of ROS scavengers that block the release of ROS, we were able to demonstrate that inhibition of autophagy increases cell survival.

CONCLUSIONS:

The study suggests that ROS accumulation is involved in the sI/R-induced autophagic cell death in HUVECs.

PMID:
24943908
PMCID:
PMC4074109
DOI:
10.12659/MSM.890897
[Indexed for MEDLINE]
Free PMC Article
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