Cargando…

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...

Descripción completa

Detalles Bibliográficos
Autores principales: Cai, Yuhua, Li, Yunpeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
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
_version_ 1783410342204801024
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