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The Role of MicroRNA-181a in Myocardial Fibrosis Following Myocardial Infarction in a Rat Model
BACKGROUND: The role of miR-181a in the development of cardiac disease and in particular, myocardial fibrosis following myocardial infarction (MI) remains unknown. The aim of this study was to explore the role of miR-181a in myocardial fibrosis in a rat model of MI and the expression of TGF-β recept...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6036961/ https://www.ncbi.nlm.nih.gov/pubmed/29908129 http://dx.doi.org/10.12659/MSM.908056 |
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author | Chen, Peng Pan, Jialin Zhang, Xinming Shi, Zhewei Yang, Xiangjun |
author_facet | Chen, Peng Pan, Jialin Zhang, Xinming Shi, Zhewei Yang, Xiangjun |
author_sort | Chen, Peng |
collection | PubMed |
description | BACKGROUND: The role of miR-181a in the development of cardiac disease and in particular, myocardial fibrosis following myocardial infarction (MI) remains unknown. The aim of this study was to explore the role of miR-181a in myocardial fibrosis in a rat model of MI and the expression of TGF-β receptor III (TβRIII). MATERIAL/METHODS: Forty adult male Wistar rats were randomly divided into an MI model group (n=30) and a control group with (n=10). The rat MI model involved ligating the left anterior descending (LAD) coronary artery in the model group; the control group was treated with a sham operation. Cardiac function was assessed using cardiac ultrasound. Myocardial fibroblasts were extracted from the rat hearts and transfected with a miR-mimic or miR-inhibitor, and cell growth was measured using an MTT assay. The level of miR-181a expression was detected using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blots. RESULTS: miR-181a expression was significantly increased during the progression of MI (P<0.05). Over-expression of miR-181a was associated with increased deposition of extracellular matrix (ECM) components, collagen I and fibronectin. This effect was reversed with the use of a miR-181a inhibitor (P<0.05). Upregulation of miR-181a suppressed the expression of TGF-β receptor III (TβRIII) by binding with 3′-UTR. CONCLUSIONS: In this rat model of MI, the findings were that miR-181a had a role in the progression of myocardial fibrosis. The findings require further studies to determine whether miR-181a might provide a novel therapeutic target to limit myocardial fibrosis following MI. |
format | Online Article Text |
id | pubmed-6036961 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-60369612018-07-11 The Role of MicroRNA-181a in Myocardial Fibrosis Following Myocardial Infarction in a Rat Model Chen, Peng Pan, Jialin Zhang, Xinming Shi, Zhewei Yang, Xiangjun Med Sci Monit Lab/In Vitro Research BACKGROUND: The role of miR-181a in the development of cardiac disease and in particular, myocardial fibrosis following myocardial infarction (MI) remains unknown. The aim of this study was to explore the role of miR-181a in myocardial fibrosis in a rat model of MI and the expression of TGF-β receptor III (TβRIII). MATERIAL/METHODS: Forty adult male Wistar rats were randomly divided into an MI model group (n=30) and a control group with (n=10). The rat MI model involved ligating the left anterior descending (LAD) coronary artery in the model group; the control group was treated with a sham operation. Cardiac function was assessed using cardiac ultrasound. Myocardial fibroblasts were extracted from the rat hearts and transfected with a miR-mimic or miR-inhibitor, and cell growth was measured using an MTT assay. The level of miR-181a expression was detected using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blots. RESULTS: miR-181a expression was significantly increased during the progression of MI (P<0.05). Over-expression of miR-181a was associated with increased deposition of extracellular matrix (ECM) components, collagen I and fibronectin. This effect was reversed with the use of a miR-181a inhibitor (P<0.05). Upregulation of miR-181a suppressed the expression of TGF-β receptor III (TβRIII) by binding with 3′-UTR. CONCLUSIONS: In this rat model of MI, the findings were that miR-181a had a role in the progression of myocardial fibrosis. The findings require further studies to determine whether miR-181a might provide a novel therapeutic target to limit myocardial fibrosis following MI. International Scientific Literature, Inc. 2018-06-16 /pmc/articles/PMC6036961/ /pubmed/29908129 http://dx.doi.org/10.12659/MSM.908056 Text en © Med Sci Monit, 2018 This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) ) |
spellingShingle | Lab/In Vitro Research Chen, Peng Pan, Jialin Zhang, Xinming Shi, Zhewei Yang, Xiangjun The Role of MicroRNA-181a in Myocardial Fibrosis Following Myocardial Infarction in a Rat Model |
title | The Role of MicroRNA-181a in Myocardial Fibrosis Following Myocardial Infarction in a Rat Model |
title_full | The Role of MicroRNA-181a in Myocardial Fibrosis Following Myocardial Infarction in a Rat Model |
title_fullStr | The Role of MicroRNA-181a in Myocardial Fibrosis Following Myocardial Infarction in a Rat Model |
title_full_unstemmed | The Role of MicroRNA-181a in Myocardial Fibrosis Following Myocardial Infarction in a Rat Model |
title_short | The Role of MicroRNA-181a in Myocardial Fibrosis Following Myocardial Infarction in a Rat Model |
title_sort | role of microrna-181a in myocardial fibrosis following myocardial infarction in a rat model |
topic | Lab/In Vitro Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6036961/ https://www.ncbi.nlm.nih.gov/pubmed/29908129 http://dx.doi.org/10.12659/MSM.908056 |
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