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microRNA-29a inhibits cardiac fibrosis in Sprague-Dawley rats by downregulating the expression of DNMT3A
OBJECTIVE: This study aims to investigate the effect of miR-29a targeting the regulation of DNMT3A on the development of cardiac fibrosis in Sprague-Dawley (SD) rats. METHODS: In vivo experiment: SD rats were randomly divided into model and control groups. The cardiac and left ventricular indices in...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Kare Publishing
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6249525/ https://www.ncbi.nlm.nih.gov/pubmed/30297596 http://dx.doi.org/10.14744/AnatolJCardiol.2018.98511 |
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author | Qin, Run-He Tao, Hui Ni, Shi-Hao Shi, Peng Dai, Chen Shi, Kai-Hu |
author_facet | Qin, Run-He Tao, Hui Ni, Shi-Hao Shi, Peng Dai, Chen Shi, Kai-Hu |
author_sort | Qin, Run-He |
collection | PubMed |
description | OBJECTIVE: This study aims to investigate the effect of miR-29a targeting the regulation of DNMT3A on the development of cardiac fibrosis in Sprague-Dawley (SD) rats. METHODS: In vivo experiment: SD rats were randomly divided into model and control groups. The cardiac and left ventricular indices in each group were calculated. The pathological changes of the myocardium were observed. The expression levels of miR-29a, CollA1, α-SMA, and DNMT3A in the myocardium of each group were detected. In vitro experiment: The cardiac fibroblasts (CFs) of SD rats were isolated from the myocardial tissue of SD rats and cultured. The miR-29a mimics, inhibitors, DNMT3A-siRNA, and control-siRNA were transfected into CFs. The expression levels of miR-29a, DNMT3A, CollA1, and α-SMA were detected, and the proliferation of CFs after transfection was observed. RESULTS: The heart weight index of the rats in the model group increased significantly compared with that in the control group. Obvious collagen deposition was observed in the myocardial tissue of the model group. The expression levels of CollA1, α-SMA, and DNMT3A in the model group were significantly higher than those in the control group (p<0.05). CONCLUSION: miR-29a reduced the activation and proliferation of CFs to improve cardiac fibrosis probably by the downregulation of DNMT3A. |
format | Online Article Text |
id | pubmed-6249525 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Kare Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-62495252018-12-20 microRNA-29a inhibits cardiac fibrosis in Sprague-Dawley rats by downregulating the expression of DNMT3A Qin, Run-He Tao, Hui Ni, Shi-Hao Shi, Peng Dai, Chen Shi, Kai-Hu Anatol J Cardiol Original Investigation OBJECTIVE: This study aims to investigate the effect of miR-29a targeting the regulation of DNMT3A on the development of cardiac fibrosis in Sprague-Dawley (SD) rats. METHODS: In vivo experiment: SD rats were randomly divided into model and control groups. The cardiac and left ventricular indices in each group were calculated. The pathological changes of the myocardium were observed. The expression levels of miR-29a, CollA1, α-SMA, and DNMT3A in the myocardium of each group were detected. In vitro experiment: The cardiac fibroblasts (CFs) of SD rats were isolated from the myocardial tissue of SD rats and cultured. The miR-29a mimics, inhibitors, DNMT3A-siRNA, and control-siRNA were transfected into CFs. The expression levels of miR-29a, DNMT3A, CollA1, and α-SMA were detected, and the proliferation of CFs after transfection was observed. RESULTS: The heart weight index of the rats in the model group increased significantly compared with that in the control group. Obvious collagen deposition was observed in the myocardial tissue of the model group. The expression levels of CollA1, α-SMA, and DNMT3A in the model group were significantly higher than those in the control group (p<0.05). CONCLUSION: miR-29a reduced the activation and proliferation of CFs to improve cardiac fibrosis probably by the downregulation of DNMT3A. Kare Publishing 2018-10 2018-09-11 /pmc/articles/PMC6249525/ /pubmed/30297596 http://dx.doi.org/10.14744/AnatolJCardiol.2018.98511 Text en Copyright: © 2018 Turkish Society of Cardiology http://creativecommons.org/licenses/by-nc-sa/4.0 This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License |
spellingShingle | Original Investigation Qin, Run-He Tao, Hui Ni, Shi-Hao Shi, Peng Dai, Chen Shi, Kai-Hu microRNA-29a inhibits cardiac fibrosis in Sprague-Dawley rats by downregulating the expression of DNMT3A |
title | microRNA-29a inhibits cardiac fibrosis in Sprague-Dawley rats by downregulating the expression of DNMT3A |
title_full | microRNA-29a inhibits cardiac fibrosis in Sprague-Dawley rats by downregulating the expression of DNMT3A |
title_fullStr | microRNA-29a inhibits cardiac fibrosis in Sprague-Dawley rats by downregulating the expression of DNMT3A |
title_full_unstemmed | microRNA-29a inhibits cardiac fibrosis in Sprague-Dawley rats by downregulating the expression of DNMT3A |
title_short | microRNA-29a inhibits cardiac fibrosis in Sprague-Dawley rats by downregulating the expression of DNMT3A |
title_sort | microrna-29a inhibits cardiac fibrosis in sprague-dawley rats by downregulating the expression of dnmt3a |
topic | Original Investigation |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6249525/ https://www.ncbi.nlm.nih.gov/pubmed/30297596 http://dx.doi.org/10.14744/AnatolJCardiol.2018.98511 |
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