Open Access

lncRNA FGD5 antisense RNA 1 upregulates RORA to suppress hypoxic injury of human cardiomyocyte cells by inhibiting oxidative stress and apoptosis via miR‑195

  • Authors:
    • Xinyong Cai
    • Ping Zhang
    • Shu Wang
    • Lang Hong
    • Songping Yu
    • Bin Li
    • Hong Zeng
    • Xu Yang
    • Liang Shao
  • View Affiliations

  • Published online on: October 2, 2020     https://doi.org/10.3892/mmr.2020.11558
  • Pages: 4579-4588
  • Copyright: © Cai et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

FGD5 antisense RNA 1 (FGD5‑AS1) is a long non‑coding RNA in acute myocardial infarction (AMI), which is primarily caused by myocardial ischemia‑hypoxia. Retinoid acid receptor‑related orphan receptor α (RORA) is a key protector in maintaining heart function. However, the roles of FGD5‑AS1 and RORA in AMI have not previously been elucidated. The present study investigated the effect and mechanism of FGD5‑AS1 and RORA in human cardiomyocyte AC16 cells under hypoxia. Reverse transcription‑quantitative PCR and western blotting demonstrated that FGD5‑AS1 and RORA were downregulated in the serum of patients with AMI and hypoxia‑challenged AC16 cells. Functional experiments were performed via assays, flow cytometry and western blotting. In response to hypoxia, superoxide dismutase (SOD) activity was inhibited, but apoptosis rate and levels of reactive oxygen species and malondialdehyde were promoted in AC16 cells, accompanied by increased Bax and cleaved caspase‑3 expression levels, and decreased SOD2 and glutathione peroxidase 1 expression levels. However, hypoxia‑induced oxidative stress and apoptosis in AC16 cells were attenuated by ectopic expression of FGD5‑AS1 or RORA. Moreover, silencing RORA counteracted the suppressive role of FGD5‑AS1 overexpression in hypoxic injury. FGD5‑AS1 controlled RORA expression levels via microRNA‑195‑5p (miR‑195), as confirmed by dual‑luciferase reporter and RNA pull‑down assays. Consistently, miR‑195 knockdown suppressed hypoxia‑induced oxidative stress and apoptosis in AC16 cells, which was abrogated by downregulating FGD5‑AS1 or RORA. In conclusion, FGD5‑AS1 modulated hypoxic injury in human cardiomyocytes partially via the miR‑195/RORA axis, suggesting FGD5‑AS1 as a potential target in interfering with the progression of AMI.
View Figures
View References

Related Articles

Journal Cover

December-2020
Volume 22 Issue 6

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
Cai X, Zhang P, Wang S, Hong L, Yu S, Li B, Zeng H, Yang X and Shao L: lncRNA FGD5 antisense RNA 1 upregulates RORA to suppress hypoxic injury of human cardiomyocyte cells by inhibiting oxidative stress and apoptosis via miR‑195. Mol Med Rep 22: 4579-4588, 2020
APA
Cai, X., Zhang, P., Wang, S., Hong, L., Yu, S., Li, B. ... Shao, L. (2020). lncRNA FGD5 antisense RNA 1 upregulates RORA to suppress hypoxic injury of human cardiomyocyte cells by inhibiting oxidative stress and apoptosis via miR‑195. Molecular Medicine Reports, 22, 4579-4588. https://doi.org/10.3892/mmr.2020.11558
MLA
Cai, X., Zhang, P., Wang, S., Hong, L., Yu, S., Li, B., Zeng, H., Yang, X., Shao, L."lncRNA FGD5 antisense RNA 1 upregulates RORA to suppress hypoxic injury of human cardiomyocyte cells by inhibiting oxidative stress and apoptosis via miR‑195". Molecular Medicine Reports 22.6 (2020): 4579-4588.
Chicago
Cai, X., Zhang, P., Wang, S., Hong, L., Yu, S., Li, B., Zeng, H., Yang, X., Shao, L."lncRNA FGD5 antisense RNA 1 upregulates RORA to suppress hypoxic injury of human cardiomyocyte cells by inhibiting oxidative stress and apoptosis via miR‑195". Molecular Medicine Reports 22, no. 6 (2020): 4579-4588. https://doi.org/10.3892/mmr.2020.11558