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Zinc finger protein 91 loss induces cardiac hypertrophy through adenosine A1 receptor down‐regulation under pressure overload status
The function of zfp91 is mainly studied in vitro, but there is no study in vivo. Accumulative data suggest that zfp91 may be an important gene to regulate all aspects of human response. However, there are no data to date about the function of zfp91 on cardiac homeostasis. Thus, we aimed to observe t...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7520255/ https://www.ncbi.nlm.nih.gov/pubmed/32677376 http://dx.doi.org/10.1111/jcmm.15630 |
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author | Wu, Xiangqi You, Wei Wu, Zhiming Ye, Fei Chen, Shaoliang |
author_facet | Wu, Xiangqi You, Wei Wu, Zhiming Ye, Fei Chen, Shaoliang |
author_sort | Wu, Xiangqi |
collection | PubMed |
description | The function of zfp91 is mainly studied in vitro, but there is no study in vivo. Accumulative data suggest that zfp91 may be an important gene to regulate all aspects of human response. However, there are no data to date about the function of zfp91 on cardiac homeostasis. Thus, we aimed to observe the role of zfp91 gene in mouse cardiomyocytes on myocardial homeostasis and related mechanisms under pressure overload. In the study, zfp91 mRNA and protein levels were significantly reduced in TAC‐operated WT mice as compared with controls. Genetic ablation of zfp91 dramatically led to pathological cardiac dysfunction and hypertrophy after transverse aortic constriction (TAC). Adenosine A1 receptor (Adora1) mRNA and protein expressions were significantly down‐regulated in the heart of zfp91‐deletion mice with TAC. Zfp91 overexpression reversed isoproterenol‐induced cardiomyocyte hypertrophy, which was abolished by selective Adora1 antagonist. Dual‐luciferase reporter and ChIP‐qPCR assays indicated that zfp91 acted on Adora1 promoter through its binding site. Last, Adora1 agonist rescued heart dysfunction and cardiac hypertrophy in zfp91 loss mice after TAC. Zfp91 may transcriptionally regulate Adora1 expression in the heart, which mainly maintained cardiac homeostasis under pressure overload status. It will provide a new approach to treat cardiac hypertrophy. |
format | Online Article Text |
id | pubmed-7520255 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-75202552020-09-30 Zinc finger protein 91 loss induces cardiac hypertrophy through adenosine A1 receptor down‐regulation under pressure overload status Wu, Xiangqi You, Wei Wu, Zhiming Ye, Fei Chen, Shaoliang J Cell Mol Med Original Articles The function of zfp91 is mainly studied in vitro, but there is no study in vivo. Accumulative data suggest that zfp91 may be an important gene to regulate all aspects of human response. However, there are no data to date about the function of zfp91 on cardiac homeostasis. Thus, we aimed to observe the role of zfp91 gene in mouse cardiomyocytes on myocardial homeostasis and related mechanisms under pressure overload. In the study, zfp91 mRNA and protein levels were significantly reduced in TAC‐operated WT mice as compared with controls. Genetic ablation of zfp91 dramatically led to pathological cardiac dysfunction and hypertrophy after transverse aortic constriction (TAC). Adenosine A1 receptor (Adora1) mRNA and protein expressions were significantly down‐regulated in the heart of zfp91‐deletion mice with TAC. Zfp91 overexpression reversed isoproterenol‐induced cardiomyocyte hypertrophy, which was abolished by selective Adora1 antagonist. Dual‐luciferase reporter and ChIP‐qPCR assays indicated that zfp91 acted on Adora1 promoter through its binding site. Last, Adora1 agonist rescued heart dysfunction and cardiac hypertrophy in zfp91 loss mice after TAC. Zfp91 may transcriptionally regulate Adora1 expression in the heart, which mainly maintained cardiac homeostasis under pressure overload status. It will provide a new approach to treat cardiac hypertrophy. John Wiley and Sons Inc. 2020-07-17 2020-09 /pmc/articles/PMC7520255/ /pubmed/32677376 http://dx.doi.org/10.1111/jcmm.15630 Text en © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Wu, Xiangqi You, Wei Wu, Zhiming Ye, Fei Chen, Shaoliang Zinc finger protein 91 loss induces cardiac hypertrophy through adenosine A1 receptor down‐regulation under pressure overload status |
title | Zinc finger protein 91 loss induces cardiac hypertrophy through adenosine A1 receptor down‐regulation under pressure overload status |
title_full | Zinc finger protein 91 loss induces cardiac hypertrophy through adenosine A1 receptor down‐regulation under pressure overload status |
title_fullStr | Zinc finger protein 91 loss induces cardiac hypertrophy through adenosine A1 receptor down‐regulation under pressure overload status |
title_full_unstemmed | Zinc finger protein 91 loss induces cardiac hypertrophy through adenosine A1 receptor down‐regulation under pressure overload status |
title_short | Zinc finger protein 91 loss induces cardiac hypertrophy through adenosine A1 receptor down‐regulation under pressure overload status |
title_sort | zinc finger protein 91 loss induces cardiac hypertrophy through adenosine a1 receptor down‐regulation under pressure overload status |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7520255/ https://www.ncbi.nlm.nih.gov/pubmed/32677376 http://dx.doi.org/10.1111/jcmm.15630 |
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