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Upregulation of miR-29b-3p protects cardiomyocytes from hypoxia-induced apoptosis by targeting TRAF5
BACKGROUND: MicroRNAs (miRNAs) are pivotal regulators in regulating hypoxia-induced cardiomyocyte injury. This study was designed to evaluate the effects of miR-29b-3p on hypoxic cardiomyocytes. METHODS: Human AC16 cells were cultured under normoxic or hypoxic conditions. Hypoxic injury was confirme...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6460541/ https://www.ncbi.nlm.nih.gov/pubmed/31011336 http://dx.doi.org/10.1186/s11658-019-0151-3 |
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author | Cai, Yuhua Li, Yunpeng |
author_facet | Cai, Yuhua Li, Yunpeng |
author_sort | Cai, Yuhua |
collection | PubMed |
description | BACKGROUND: MicroRNAs (miRNAs) are pivotal regulators in regulating hypoxia-induced cardiomyocyte injury. This study was designed to evaluate the effects of miR-29b-3p on hypoxic cardiomyocytes. METHODS: Human AC16 cells were cultured under normoxic or hypoxic conditions. Hypoxic injury was confirmed based on alterations in cell viability using CCK-8 assay and apoptosis using flow cytometry and Hoechst staining. Bioinformatics analyses and the dual-luciferase reporter assay were performed to predict and validate the target gene of miR-29b-3p. RESULTS: We found that hypoxia suppressed cell viability and promoted apoptosis. TNF receptor-associated factor 5 (TRAF5) was a potential target gene of miR-29b-3p. Our in vitro experiments revealed that miR-29b-3p overexpression or TRAF6 knockdown significantly protected cardiomyocytes against hypoxia-induced injury. Moreover, knockdown of TRAF5 knockdown potentiated the protective effects of miR-29b-3p against hypoxia-induced cell injury. CONCLUSION: These findings suggest that upregulation of miR-29b-3p could protect cardiomyocytes against hypoxia-induced injury through downregulation of TRAF5. Targeting TRAF5 with miR-29b-3p might be a potential therapeutic method for AMI. |
format | Online Article Text |
id | pubmed-6460541 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-64605412019-04-22 Upregulation of miR-29b-3p protects cardiomyocytes from hypoxia-induced apoptosis by targeting TRAF5 Cai, Yuhua Li, Yunpeng Cell Mol Biol Lett Research Letter BACKGROUND: MicroRNAs (miRNAs) are pivotal regulators in regulating hypoxia-induced cardiomyocyte injury. This study was designed to evaluate the effects of miR-29b-3p on hypoxic cardiomyocytes. METHODS: Human AC16 cells were cultured under normoxic or hypoxic conditions. Hypoxic injury was confirmed based on alterations in cell viability using CCK-8 assay and apoptosis using flow cytometry and Hoechst staining. Bioinformatics analyses and the dual-luciferase reporter assay were performed to predict and validate the target gene of miR-29b-3p. RESULTS: We found that hypoxia suppressed cell viability and promoted apoptosis. TNF receptor-associated factor 5 (TRAF5) was a potential target gene of miR-29b-3p. Our in vitro experiments revealed that miR-29b-3p overexpression or TRAF6 knockdown significantly protected cardiomyocytes against hypoxia-induced injury. Moreover, knockdown of TRAF5 knockdown potentiated the protective effects of miR-29b-3p against hypoxia-induced cell injury. CONCLUSION: These findings suggest that upregulation of miR-29b-3p could protect cardiomyocytes against hypoxia-induced injury through downregulation of TRAF5. Targeting TRAF5 with miR-29b-3p might be a potential therapeutic method for AMI. BioMed Central 2019-04-11 /pmc/articles/PMC6460541/ /pubmed/31011336 http://dx.doi.org/10.1186/s11658-019-0151-3 Text en © The Author(s) 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Letter Cai, Yuhua Li, Yunpeng Upregulation of miR-29b-3p protects cardiomyocytes from hypoxia-induced apoptosis by targeting TRAF5 |
title | Upregulation of miR-29b-3p protects cardiomyocytes from hypoxia-induced apoptosis by targeting TRAF5 |
title_full | Upregulation of miR-29b-3p protects cardiomyocytes from hypoxia-induced apoptosis by targeting TRAF5 |
title_fullStr | Upregulation of miR-29b-3p protects cardiomyocytes from hypoxia-induced apoptosis by targeting TRAF5 |
title_full_unstemmed | Upregulation of miR-29b-3p protects cardiomyocytes from hypoxia-induced apoptosis by targeting TRAF5 |
title_short | Upregulation of miR-29b-3p protects cardiomyocytes from hypoxia-induced apoptosis by targeting TRAF5 |
title_sort | upregulation of mir-29b-3p protects cardiomyocytes from hypoxia-induced apoptosis by targeting traf5 |
topic | Research Letter |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6460541/ https://www.ncbi.nlm.nih.gov/pubmed/31011336 http://dx.doi.org/10.1186/s11658-019-0151-3 |
work_keys_str_mv | AT caiyuhua upregulationofmir29b3pprotectscardiomyocytesfromhypoxiainducedapoptosisbytargetingtraf5 AT liyunpeng upregulationofmir29b3pprotectscardiomyocytesfromhypoxiainducedapoptosisbytargetingtraf5 |