ArticleExperimental and therapeutic medicine2020
Downregulation of miRNA-663b protects against hypoxia-induced injury in cardiomyocytes by targeting BCL2L1.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Harnessing miRNA therapeutics: a novel approach to combat heart and brain infarctions in atherosclerosis.Cell death discovery · 2025Review
- Restoration of miR-650 leads to down-regulation of KISS1, a possible route involved in overcoming 5-FU resistance and induction of apoptosis in CRC cells in-vitro.Molecular biology reports · 2023Article
- Article
- The active ingredient (DSH-20) of Salvia miltiorrhiza flower reduces oxidative damage and apoptosis in cardiomyocytes by regulating miR-1.Molecular biology reports · 2022Article
- Exosomal miR‑663b exposed to TGF‑β1 promotes cervical cancer metastasis and epithelial‑mesenchymal transition by targeting MGAT3.Oncology reports · 2021Article
- The Regulation Mechanisms and Clinical Application of MicroRNAs in Myocardial Infarction: A Review of the Recent 5 Years.Frontiers in cardiovascular medicine · 2021Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study, the role of microRNA-663b (miR-663b) in cardiomyocyte injury was examined. Reverse transcription-quantitative PCR (RT-qPCR) was performed to detect miR-663b expression in hypoxia-induced H9c2 cells. The results revealed that miR-663b expression was significantly upregulated in hypoxia-induced H9c2 cells compared with control cells. TargetScan analysis and dual-luciferase reporter assays demonstrated that miR-663b directly targeted the B-cell lymphoma 2 like 1 (BCL2L1) gene. RT-qPCR and western blotting data indicated that BCL2L1 expression was significantly downregulated in hypoxia-induced H9c2 cells compared with control cells. Under hypoxic conditions, H9c2 cells were transfected with miR-663b inhibitor, inhibitor control, miR-663b inhibitor + control small interfering (si)RNA or miR-663b inhibitor + BCL2L1-siRNA for 48 h. ELISA against creatine kinase-muscle/brain (CK-MB) and cardiac troponin 1 (cTnI) demonstrated that the miR-663b inhibitor reduced CK-MD and cTnI release and increased mitochondrial viability when compared with hypoxia-treated cells. Additionally, the miR-663b inhibitor significantly increased H9c2 cell viability and decreased cell apoptosis under hypoxic conditions. The results of ELISA further revealed that the miR-663b inhibitor decreased the release of various inflammatory factors, including tumour necrosis factor α, interleukin (IL) 1β and IL-6 in H9c2 cells under hypoxic conditions. These changes were reversed following BCL2L1 knockdown. In conclusion, miR-663b inhibition protected cardiomyocytes against hypoxia-induced injury by targeting BCL2L1 and may potentially be a novel target for the treatment of patients with myocardial infarction.
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