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miR-214-3p Protects and Restores the Myocardial Tissue of Rat Myocardial Infarction Model by Targeting PTEN

Myocardial infarction (MI), which results in myocardial cell dysfunction and irreversible loss, is one of the most serious health threats today. This study was started with rats, by which the consequence of miRNA expression dysregulation to the occurrence and progression of cardiovascular diseases w...

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Autores principales: Cheng, Yuan, He, Qing, Jin, Tao, Li, Na
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9313954/
https://www.ncbi.nlm.nih.gov/pubmed/35899226
http://dx.doi.org/10.1155/2022/1175935
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author Cheng, Yuan
He, Qing
Jin, Tao
Li, Na
author_facet Cheng, Yuan
He, Qing
Jin, Tao
Li, Na
author_sort Cheng, Yuan
collection PubMed
description Myocardial infarction (MI), which results in myocardial cell dysfunction and irreversible loss, is one of the most serious health threats today. This study was started with rats, by which the consequence of miRNA expression dysregulation to the occurrence and progression of cardiovascular diseases was explored. We first conducted miRNA sequencing on the myocardial tissues separately from myocardial infarction treatment and sham operation treatment to clarify those differently expressed miRNAs; then, our experiment of functional verification of those key miRNAs was initiated so as to dig out the molecular mechanism behind the miRNA's regulation in myocardial infarction. And it turned out that there were 32 upregulated miRNAs and 16 downregulated miRNAs according to our comparison from the myocardial infarction model group to the sham operation group; of all those upregulated, alteration in miR-214-3p expression was the most conspicuous. Overexpression of miR-214-3p greatly alleviated myocardial infarct area and ameliorated myocardial tissue structure, even reducing myocardial fibrosis and the devastation in the tissues. On the molecular level, miR-214-3p overexpression brought down both the apoptosis rate and cleaved caspase 3 expression. Besides that, we verified that PTEN is the target gene of miR-214-3p through a dual-luciferase assay. A cotransfection of miR-214-3p and PTEN brought about an obvious elevation in the myocardial infarct area, tissue damage, and fibrosis, even in the aspect of cellular apoptosis than a mere transfection of miR-214-3p. All the results above verified miR-214-3p′s effects in protecting myocardial tissues and reducing the infarct area, and it was reasonable to assume that those functions of miR-214-3p came into effect by targeting PTEN, which was then justified by the inversion to miR-214-3p′s protection via PTEN overexpression.
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spelling pubmed-93139542022-07-26 miR-214-3p Protects and Restores the Myocardial Tissue of Rat Myocardial Infarction Model by Targeting PTEN Cheng, Yuan He, Qing Jin, Tao Li, Na Evid Based Complement Alternat Med Research Article Myocardial infarction (MI), which results in myocardial cell dysfunction and irreversible loss, is one of the most serious health threats today. This study was started with rats, by which the consequence of miRNA expression dysregulation to the occurrence and progression of cardiovascular diseases was explored. We first conducted miRNA sequencing on the myocardial tissues separately from myocardial infarction treatment and sham operation treatment to clarify those differently expressed miRNAs; then, our experiment of functional verification of those key miRNAs was initiated so as to dig out the molecular mechanism behind the miRNA's regulation in myocardial infarction. And it turned out that there were 32 upregulated miRNAs and 16 downregulated miRNAs according to our comparison from the myocardial infarction model group to the sham operation group; of all those upregulated, alteration in miR-214-3p expression was the most conspicuous. Overexpression of miR-214-3p greatly alleviated myocardial infarct area and ameliorated myocardial tissue structure, even reducing myocardial fibrosis and the devastation in the tissues. On the molecular level, miR-214-3p overexpression brought down both the apoptosis rate and cleaved caspase 3 expression. Besides that, we verified that PTEN is the target gene of miR-214-3p through a dual-luciferase assay. A cotransfection of miR-214-3p and PTEN brought about an obvious elevation in the myocardial infarct area, tissue damage, and fibrosis, even in the aspect of cellular apoptosis than a mere transfection of miR-214-3p. All the results above verified miR-214-3p′s effects in protecting myocardial tissues and reducing the infarct area, and it was reasonable to assume that those functions of miR-214-3p came into effect by targeting PTEN, which was then justified by the inversion to miR-214-3p′s protection via PTEN overexpression. Hindawi 2022-07-18 /pmc/articles/PMC9313954/ /pubmed/35899226 http://dx.doi.org/10.1155/2022/1175935 Text en Copyright © 2022 Yuan Cheng et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Cheng, Yuan
He, Qing
Jin, Tao
Li, Na
miR-214-3p Protects and Restores the Myocardial Tissue of Rat Myocardial Infarction Model by Targeting PTEN
title miR-214-3p Protects and Restores the Myocardial Tissue of Rat Myocardial Infarction Model by Targeting PTEN
title_full miR-214-3p Protects and Restores the Myocardial Tissue of Rat Myocardial Infarction Model by Targeting PTEN
title_fullStr miR-214-3p Protects and Restores the Myocardial Tissue of Rat Myocardial Infarction Model by Targeting PTEN
title_full_unstemmed miR-214-3p Protects and Restores the Myocardial Tissue of Rat Myocardial Infarction Model by Targeting PTEN
title_short miR-214-3p Protects and Restores the Myocardial Tissue of Rat Myocardial Infarction Model by Targeting PTEN
title_sort mir-214-3p protects and restores the myocardial tissue of rat myocardial infarction model by targeting pten
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9313954/
https://www.ncbi.nlm.nih.gov/pubmed/35899226
http://dx.doi.org/10.1155/2022/1175935
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