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LncRNA LINC00461 exacerbates myocardial ischemia–reperfusion injury via microRNA-185-3p/Myd88
OBJECTIVE: Long non-coding RNAs (lncRNAs) play critically in the pathogenesis of myocardial ischemia–reperfusion (I/R) injury. Thus, it was proposed to investigate the mechanism of LINC00461 in the disease through mediating microRNA-185-3p (miR-185-3p)/myeloid differentiation primary response gene 8...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8908691/ https://www.ncbi.nlm.nih.gov/pubmed/35272621 http://dx.doi.org/10.1186/s10020-022-00452-1 |
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author | Gao, Feng Wang, Xiaochen Fan, Tingting Luo, Zhidan Ma, Mengqing Hu, Guangquan Li, Yue Liang, Yi Lin, Xianhe Xu, Banglong |
author_facet | Gao, Feng Wang, Xiaochen Fan, Tingting Luo, Zhidan Ma, Mengqing Hu, Guangquan Li, Yue Liang, Yi Lin, Xianhe Xu, Banglong |
author_sort | Gao, Feng |
collection | PubMed |
description | OBJECTIVE: Long non-coding RNAs (lncRNAs) play critically in the pathogenesis of myocardial ischemia–reperfusion (I/R) injury. Thus, it was proposed to investigate the mechanism of LINC00461 in the disease through mediating microRNA-185-3p (miR-185-3p)/myeloid differentiation primary response gene 88 (Myd88) axis. METHODS: miR-185-3p, LINC00461 and Myd88 expression in mice with I/R injury was measured. Mice with I/R injury were injected with the gene expression-modified vectors, after which cardiac function, hemodynamics, myocardial enzyme, oxidative stress, and cardiomyocyte apoptosis were analyzed. RESULTS: I/R mice showed LINC00461 and Myd88 up-regulation and miR-185-3p down-regulation. Down-regulating LINC00461 or up-regulating miR-185-3p recovered cardiac function, reduced myocardial enzyme levels, and attenuated oxidative stress and cardiomyocyte apoptosis in mice with I/R. miR-185-3p overexpression rescued the promoting effect of LINC00461 upregulation on myocardial injury in I/R mice. CONCLUSION: LINC00461 knockdown attenuates myocardial I/R injury via elevating miR-185-3p expression to suppress Myd88 expression. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s10020-022-00452-1. |
format | Online Article Text |
id | pubmed-8908691 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-89086912022-03-18 LncRNA LINC00461 exacerbates myocardial ischemia–reperfusion injury via microRNA-185-3p/Myd88 Gao, Feng Wang, Xiaochen Fan, Tingting Luo, Zhidan Ma, Mengqing Hu, Guangquan Li, Yue Liang, Yi Lin, Xianhe Xu, Banglong Mol Med Research Article OBJECTIVE: Long non-coding RNAs (lncRNAs) play critically in the pathogenesis of myocardial ischemia–reperfusion (I/R) injury. Thus, it was proposed to investigate the mechanism of LINC00461 in the disease through mediating microRNA-185-3p (miR-185-3p)/myeloid differentiation primary response gene 88 (Myd88) axis. METHODS: miR-185-3p, LINC00461 and Myd88 expression in mice with I/R injury was measured. Mice with I/R injury were injected with the gene expression-modified vectors, after which cardiac function, hemodynamics, myocardial enzyme, oxidative stress, and cardiomyocyte apoptosis were analyzed. RESULTS: I/R mice showed LINC00461 and Myd88 up-regulation and miR-185-3p down-regulation. Down-regulating LINC00461 or up-regulating miR-185-3p recovered cardiac function, reduced myocardial enzyme levels, and attenuated oxidative stress and cardiomyocyte apoptosis in mice with I/R. miR-185-3p overexpression rescued the promoting effect of LINC00461 upregulation on myocardial injury in I/R mice. CONCLUSION: LINC00461 knockdown attenuates myocardial I/R injury via elevating miR-185-3p expression to suppress Myd88 expression. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s10020-022-00452-1. BioMed Central 2022-03-10 /pmc/articles/PMC8908691/ /pubmed/35272621 http://dx.doi.org/10.1186/s10020-022-00452-1 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research Article Gao, Feng Wang, Xiaochen Fan, Tingting Luo, Zhidan Ma, Mengqing Hu, Guangquan Li, Yue Liang, Yi Lin, Xianhe Xu, Banglong LncRNA LINC00461 exacerbates myocardial ischemia–reperfusion injury via microRNA-185-3p/Myd88 |
title | LncRNA LINC00461 exacerbates myocardial ischemia–reperfusion injury via microRNA-185-3p/Myd88 |
title_full | LncRNA LINC00461 exacerbates myocardial ischemia–reperfusion injury via microRNA-185-3p/Myd88 |
title_fullStr | LncRNA LINC00461 exacerbates myocardial ischemia–reperfusion injury via microRNA-185-3p/Myd88 |
title_full_unstemmed | LncRNA LINC00461 exacerbates myocardial ischemia–reperfusion injury via microRNA-185-3p/Myd88 |
title_short | LncRNA LINC00461 exacerbates myocardial ischemia–reperfusion injury via microRNA-185-3p/Myd88 |
title_sort | lncrna linc00461 exacerbates myocardial ischemia–reperfusion injury via microrna-185-3p/myd88 |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8908691/ https://www.ncbi.nlm.nih.gov/pubmed/35272621 http://dx.doi.org/10.1186/s10020-022-00452-1 |
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