lncRNA FGD5 antisense RNA 1 upregulates RORA to suppress hypoxic injury of human cardiomyocyte cells by inhibiting oxidative stress and apoptosis via miR‑195
| العنوان: | lncRNA FGD5 antisense RNA 1 upregulates RORA to suppress hypoxic injury of human cardiomyocyte cells by inhibiting oxidative stress and apoptosis via miR‑195 |
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| المؤلفون: | Songping Yu, Xu Yang, Cai Xinyong, Lang Hong, Hong Zeng, Liang Shao, Bin Li, Ping Zhang, Shu Wang |
| المصدر: | Molecular Medicine Reports |
| بيانات النشر: | Spandidos Publications, 2020. |
| سنة النشر: | 2020 |
| مصطلحات موضوعية: | 0301 basic medicine, Cancer Research, GPX1, microRNA-195, Myocardial Infarction, Myocardial Ischemia, SOD2, cardiomyocyte, Apoptosis, medicine.disease_cause, Biochemistry, Cell Line, 03 medical and health sciences, 0302 clinical medicine, Databases, Genetic, FGD5 antisense 1, Genetics, medicine, Guanine Nucleotide Exchange Factors, Humans, Myocytes, Cardiac, RNA, Antisense, Molecular Biology, chemistry.chemical_classification, Gene knockdown, Reactive oxygen species, Oncogene, hypoxia, Chemistry, Nuclear Receptor Subfamily 1, Group F, Member 1, Articles, Cell Hypoxia, Antisense RNA, Cell biology, MicroRNAs, Oxidative Stress, 030104 developmental biology, Oncology, 030220 oncology & carcinogenesis, retinoid acid receptor-related orphan receptor α, Molecular Medicine, RNA, Long Noncoding, Reactive Oxygen Species, Oxidative stress |
| الوصف: | 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. |
| تدمد: | 1791-3004 1791-2997 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::40bcf6a596a9039299ee6e31364ff7acTest https://doi.org/10.3892/mmr.2020.11558Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....40bcf6a596a9039299ee6e31364ff7ac |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 17913004 17912997 |
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