lncRNA ENSMUST00000134285 Increases MAPK11 Activity, Regulating Aging-Related Myocardial Apoptosis
Autor: | Jing Hua Liu, Zi Chao Cheng, Jia Yu Tian, Qian Fan, Xiao Chun Yang, Dong Hui Zhao, Ke Qiang Liu, Wayne Bond Lau, Xin-Liang Ma |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Aging Blotting Western Ischemia Apoptosis Real-Time Polymerase Chain Reaction Mice 03 medical and health sciences Mitogen-Activated Protein Kinase 11 medicine Animals MAPK11 Myocytes Cardiac Oligonucleotide Array Sequence Analysis Messenger RNA Gene knockdown TUNEL assay Chemistry Myocardium Hypoxia (medical) medicine.disease Cell biology 030104 developmental biology Gene chip analysis RNA Long Noncoding Geriatrics and Gerontology medicine.symptom |
Zdroj: | The Journals of Gerontology: Series A. 73:1010-1017 |
ISSN: | 1758-535X 1079-5006 |
DOI: | 10.1093/gerona/gly020 |
Popis: | Previous studies have demonstrated that aging promotes myocardial apoptosis after ischemia/reperfusion, via unknown specific mechanisms. The present study investigates the potential relationship between lncRNAs and aging-related apoptosis by lncRNA/mRNA microarray technology. The results indicate aging increased myocardial lncRNA ENSMUST00000134285 and mMAPK11, confirmed by both bioinformatics analysis and polymerase chain reaction (PCR). Mouse cardiomyocytes were subjected to gene manipulation (ENSMUST00000134285 knockdown and overexpression). Knockdown of ENSMUST00000134285 inhibited MAPK11 activity and increased the myocardial apoptotic ratio (determined by TUNEL staining and caspase activity assays) after hypoxia/reoxygenation. Conversely, overexpression of ENSMUST00000134285 increased MAPK11 activity and decreased the myocardial apoptotic ratio. Furthermore, luciferase reporter assay revealed that miR760 may be a mediator between ENSMUST00000134285 and mMAPK11. We have provided evidence that lncRNAs are the important regulatory molecules in aging-mediated effects upon apoptosis. The apoptosis regulatory effects of aging are complex. Except apoptosis-promoting effects, aging could also inhibit myocardial apoptosis after hypoxia or ischemia. Further studies investigating the mechanisms that aging inhibit myocardial apoptosis after hypoxia/ischemia. |
Databáze: | OpenAIRE |
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