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The Expression of microRNA in Adult Rat Heart with Isoproterenol-Induced Cardiac Hypertrophy
Cardiac hypertrophy is a common pathological condition and an independent risk factor that triggers cardiovascular morbidity. As an important epigenetic regulator, miRNA is widely involved in many biological processes. In this study, miRNAs expressed in rat hearts that underwent isoprenaline-induced...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7290591/ https://www.ncbi.nlm.nih.gov/pubmed/32397324 http://dx.doi.org/10.3390/cells9051173 |
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author | Gan, Mailin Zhang, Shunhua Fan, Yuan Tan, Ya Guo, Zhixian Chen, Lei Bai, Lin Jiang, Dongmei Hao, Xiaoxia Li, Xuewei Shen, Linyuan Zhu, Li |
author_facet | Gan, Mailin Zhang, Shunhua Fan, Yuan Tan, Ya Guo, Zhixian Chen, Lei Bai, Lin Jiang, Dongmei Hao, Xiaoxia Li, Xuewei Shen, Linyuan Zhu, Li |
author_sort | Gan, Mailin |
collection | PubMed |
description | Cardiac hypertrophy is a common pathological condition and an independent risk factor that triggers cardiovascular morbidity. As an important epigenetic regulator, miRNA is widely involved in many biological processes. In this study, miRNAs expressed in rat hearts that underwent isoprenaline-induced cardiac hypertrophy were identified using high-throughput sequencing, and functional verification of typical miRNAs was performed using rat primary cardiomyocytes. A total of 623 miRNAs were identified, of which 33 were specifically expressed in cardiac hypertrophy rats. The enriched pathways of target genes of differentially expressed miRNAs included the FoxO signaling pathway, dopaminergic synapse, Wnt signaling pathway, MAPK (mitogen-activated protein kinase) signaling pathway, and Hippo signaling pathway. Subsequently, miR-144 was the most differentially expressed miRNA and was subsequently selected for in vitro validation. Inhibition of miR-144 expression in primary myocardial cells caused up-regulation of cardiac hypertrophy markers atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). The dual luciferase reporter system showed that ANP may be a target gene of miR-144. Long non-coding RNA myocardial infarction associated transcript (LncMIAT) is closely related to heart disease, and here, we were the first to discover that LncMIAT may act as an miR-144 sponge in isoproterenol-induced cardiac hypertrophy. Taken together, these results enriched the understanding of miRNA in regulating cardiac hypertrophy and provided a reference for preventing and treating cardiac hypertrophy. |
format | Online Article Text |
id | pubmed-7290591 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-72905912020-06-17 The Expression of microRNA in Adult Rat Heart with Isoproterenol-Induced Cardiac Hypertrophy Gan, Mailin Zhang, Shunhua Fan, Yuan Tan, Ya Guo, Zhixian Chen, Lei Bai, Lin Jiang, Dongmei Hao, Xiaoxia Li, Xuewei Shen, Linyuan Zhu, Li Cells Article Cardiac hypertrophy is a common pathological condition and an independent risk factor that triggers cardiovascular morbidity. As an important epigenetic regulator, miRNA is widely involved in many biological processes. In this study, miRNAs expressed in rat hearts that underwent isoprenaline-induced cardiac hypertrophy were identified using high-throughput sequencing, and functional verification of typical miRNAs was performed using rat primary cardiomyocytes. A total of 623 miRNAs were identified, of which 33 were specifically expressed in cardiac hypertrophy rats. The enriched pathways of target genes of differentially expressed miRNAs included the FoxO signaling pathway, dopaminergic synapse, Wnt signaling pathway, MAPK (mitogen-activated protein kinase) signaling pathway, and Hippo signaling pathway. Subsequently, miR-144 was the most differentially expressed miRNA and was subsequently selected for in vitro validation. Inhibition of miR-144 expression in primary myocardial cells caused up-regulation of cardiac hypertrophy markers atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). The dual luciferase reporter system showed that ANP may be a target gene of miR-144. Long non-coding RNA myocardial infarction associated transcript (LncMIAT) is closely related to heart disease, and here, we were the first to discover that LncMIAT may act as an miR-144 sponge in isoproterenol-induced cardiac hypertrophy. Taken together, these results enriched the understanding of miRNA in regulating cardiac hypertrophy and provided a reference for preventing and treating cardiac hypertrophy. MDPI 2020-05-08 /pmc/articles/PMC7290591/ /pubmed/32397324 http://dx.doi.org/10.3390/cells9051173 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Gan, Mailin Zhang, Shunhua Fan, Yuan Tan, Ya Guo, Zhixian Chen, Lei Bai, Lin Jiang, Dongmei Hao, Xiaoxia Li, Xuewei Shen, Linyuan Zhu, Li The Expression of microRNA in Adult Rat Heart with Isoproterenol-Induced Cardiac Hypertrophy |
title | The Expression of microRNA in Adult Rat Heart with Isoproterenol-Induced Cardiac Hypertrophy |
title_full | The Expression of microRNA in Adult Rat Heart with Isoproterenol-Induced Cardiac Hypertrophy |
title_fullStr | The Expression of microRNA in Adult Rat Heart with Isoproterenol-Induced Cardiac Hypertrophy |
title_full_unstemmed | The Expression of microRNA in Adult Rat Heart with Isoproterenol-Induced Cardiac Hypertrophy |
title_short | The Expression of microRNA in Adult Rat Heart with Isoproterenol-Induced Cardiac Hypertrophy |
title_sort | expression of microrna in adult rat heart with isoproterenol-induced cardiac hypertrophy |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7290591/ https://www.ncbi.nlm.nih.gov/pubmed/32397324 http://dx.doi.org/10.3390/cells9051173 |
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