MiR-1247-3p protects rat cardiomyocytes against hypoxia/reoxygenation-induced injury via targeting BCL2L11 and caspase-2
| Autor: | Zhiyong Liao, Yiteng Huang, Xiaoqing Wang, Wenyu Guo, Zongming Feng, Jun Huang |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Cell Survival Caspase 2 Ischemia Apoptosis Protective Agents Biochemistry 03 medical and health sciences 0302 clinical medicine medicine Gene silencing Animals Humans Myocytes Cardiac Viability assay Molecular Biology Gene knockdown biology Bcl-2-Like Protein 11 Chemistry Myocardium Cell Biology Hypoxia (medical) medicine.disease Cell Hypoxia Rats MicroRNAs 030104 developmental biology BCL2L11 Gene Expression Regulation 030220 oncology & carcinogenesis Reperfusion Injury Cancer research biology.protein medicine.symptom Signal Transduction |
| Zdroj: | Journal of receptor and signal transduction research. 41(1) |
| ISSN: | 1532-4281 |
| Popis: | Acute myocardial infarction (AMI) represents a severe coronary heart disease with relatively high rate of mortality and usually can lead to the damage of the myocardial tissues. Reperfusion of the ischemic myocardial tissues can minimize AMI-induced damage. As far as we know, the molecular mechanisms underlying ischemia/reperfusion (I/R)-induced injury remains elusive. This study was undertaken to explore the role of miR-1247-3p in regulating myocardial I/R injury. The hypoxia/reoxygenation (H/R)-treated H9c2 cells showed a decreased cell viability and mitochondrial membrane potential with an increase in the apoptosis; furthermore, miR-1247-3p was down-regulated in these cells. MiR-1247-3p overexpression attenuated H/R-induced H9c2 cell injury; while miR-1247-3p knockdown in H9c2 cells exhibited similar effects being observed in H/R-treated cells. The bioinformatics prediction revealed Bcl-2-like protein 11 (BCL2L11) and caspase-2 were two potential targets for miR-1247-3p, and functional assays confirmed that miR-1247-3p targeted both BCL2L11 and caspase-2 3' untranslated regions, which lead to the repressed expression of these genes. Silencing of BCL2L11 and caspase-2 both, respectively, counteracted the H9c2 cell injury caused by H/R treatment. Moreover, BCL2L11 and caspase-2 overexpression, respectively, impaired the protective effects of miR-1247-3p overexpression on H/R-treated H9c2 cells. The data in the present investigation revealed that miR-1247-3p restoration exhibited protective effects on H/R-induced cardiomyocyte injury through targeting BCL2L11 and caspase-2, implying that miR-1247-3p along with caspase-2/BCL2L11 signaling may provide novel sight for a better understating of I/R-induced myocardial damage. The role of miR-1247-3p might be further confirmed in animal models and clinical studies. |
| Databáze: | OpenAIRE |
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