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Long noncoding RNA UCA1 inhibits ischaemia/reperfusion injury induced cardiomyocytes apoptosis via suppression of endoplasmic reticulum stress

  • Jing Chen
  • Qi Hu
  • Bo-fang Zhang
  • Xiao-pei Liu
  • Shuo Yang
  • Hong JiangEmail author
Research Article

Abstract

Background

Ischemia heart disease is one of the major causes of death worldwide which often associated with tissue infarction and limit the recovery of function. Multiple factors involved in the I/R-induced cardiomyocyte dysfunction which were consistent with a role of oxidative stress and altered endothelium-dependent responses. However, the pathogenic mechanisms in I/R injury remain unclear.

Materials and methods

The H9C2 cells were in the ischaemia/reperfusion (I/R) condition. After I/R, the cells were transfected with or without adenovirus-urothelial carcinoma associated 1(Ad-UCA1). Then qRT-PCR analysis was performed to quantify mRNA expression of different treatment groups. Cell apoptosis rate was assessed using flow cytometry and ER stress biomarker expression were measured by immunoblotting. Intracellular and mitochondrial ROS generation were assayed by fluorescence microscope after staining with the DCFDA or MitoSOX.

Results

I/R conditions trigger lncRNAs UCA1 expression, cellular and mitochondria ROS production, resulting in cell apoptosis through the induction of oxidative and ER stress. Overexpression of UCA1 protects H9C2 cells from I/R-induced ER stress and cell apoptosis. Moreover, UCA1 might be a potential regulator in the protective effect of I/R‑induced oxidative stress and mitochondria dysfunction. Subsequently, ER stress inhibitor attenuated the effect of siUCA1 induced injury in H9C2 cells.

Conclusion

The expression of UCA1 against I/R induced oxidative stress and mitochondria dysfunction via suppression of endoplasmic reticulum stress. UCA1 might be a biomarker to improved diagnosis of I/R injury.

Keywords

LncRNAs UCA1 Ischaemia/reperfusion ER stress Mitochondria dysfunction Oxidative stress 

Notes

Acknowledgements

This work was supported by the National Natural Science Foundation of China (81200156 and 81570331), and the Fundamental Research Funds for Central Universities (2042017kf0056).

Compliance with ethical standards

Conflict of interest

Jing Chen, Qi Hu, Bo-fang Zhang, Xiao-pei Liu, Shuo Yang and Hong Jiang declare that they have no conflict of interest.

Ethical approval

This study had been approved by the Renmin Hospital of Wuhan University.

Informed consent

Informed consent was obtained from all individual participants included in the study.

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Copyright information

© The Genetics Society of Korea 2019

Authors and Affiliations

  1. 1.Department of CardiologyRenmin Hospital of Wuhan UniversityWuhanChina

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