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Zinc deficiency induces abnormal development of the myocardium by promoting SENP5 overexpression
Gestational zinc deficiency is a cause of congenital heart disease in the fetus, and sentrin/small ubiquitin-like modifier (SUMO)-specific proteases (SENPs) as deSUMOylation enzymes play a crucial role in the development of cardiac structures. However, current studies of the regulation and function...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7676719/ https://www.ncbi.nlm.nih.gov/pubmed/33211757 http://dx.doi.org/10.1371/journal.pone.0242606 |
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author | Zhang, Xiaoyu Wang, Cuancuan Zhao, Dan Chen, Xuhong Zhang, Chunyan Zheng, Jun Liu, Xiaozhi |
author_facet | Zhang, Xiaoyu Wang, Cuancuan Zhao, Dan Chen, Xuhong Zhang, Chunyan Zheng, Jun Liu, Xiaozhi |
author_sort | Zhang, Xiaoyu |
collection | PubMed |
description | Gestational zinc deficiency is a cause of congenital heart disease in the fetus, and sentrin/small ubiquitin-like modifier (SUMO)-specific proteases (SENPs) as deSUMOylation enzymes play a crucial role in the development of cardiac structures. However, current studies of the regulation and function of SENP in zinc-deficient status during heart development remain limited. In this study, SUMO1 modification was found to gradually decrease during heart development, and the level of SENP5 exhibited a similar trend to SUMO1 conjugation. In addition, zinc deficiency resulted in cardiac dysplasia, increased cell apoptosis, decreased cell viability, and differentiation inhibition of hiPSC-CMs. In order to investigate the function of SENP5 in zinc deficiency, hiPSC-CMs were transfected with SENP5 small interfering RNA. The negative effects of zinc lacking conditions were reversed with depletion of SENP5. It was confirmed that zinc deficiency induced abnormal differentiation of hiPSCs and increased apoptosis of hiPSC-CMs by promoting SENP5 overexpression, which led to cardiac dysplasia. Thus, it was concluded that SENP5 regulates the SUMO1 deconjugation during heart development and zinc deficiency may reduce conjugated SUMO by promoting SENP5 overexpression, which induces abnormal development of the myocardium. |
format | Online Article Text |
id | pubmed-7676719 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-76767192020-12-02 Zinc deficiency induces abnormal development of the myocardium by promoting SENP5 overexpression Zhang, Xiaoyu Wang, Cuancuan Zhao, Dan Chen, Xuhong Zhang, Chunyan Zheng, Jun Liu, Xiaozhi PLoS One Research Article Gestational zinc deficiency is a cause of congenital heart disease in the fetus, and sentrin/small ubiquitin-like modifier (SUMO)-specific proteases (SENPs) as deSUMOylation enzymes play a crucial role in the development of cardiac structures. However, current studies of the regulation and function of SENP in zinc-deficient status during heart development remain limited. In this study, SUMO1 modification was found to gradually decrease during heart development, and the level of SENP5 exhibited a similar trend to SUMO1 conjugation. In addition, zinc deficiency resulted in cardiac dysplasia, increased cell apoptosis, decreased cell viability, and differentiation inhibition of hiPSC-CMs. In order to investigate the function of SENP5 in zinc deficiency, hiPSC-CMs were transfected with SENP5 small interfering RNA. The negative effects of zinc lacking conditions were reversed with depletion of SENP5. It was confirmed that zinc deficiency induced abnormal differentiation of hiPSCs and increased apoptosis of hiPSC-CMs by promoting SENP5 overexpression, which led to cardiac dysplasia. Thus, it was concluded that SENP5 regulates the SUMO1 deconjugation during heart development and zinc deficiency may reduce conjugated SUMO by promoting SENP5 overexpression, which induces abnormal development of the myocardium. Public Library of Science 2020-11-19 /pmc/articles/PMC7676719/ /pubmed/33211757 http://dx.doi.org/10.1371/journal.pone.0242606 Text en © 2020 Zhang et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Zhang, Xiaoyu Wang, Cuancuan Zhao, Dan Chen, Xuhong Zhang, Chunyan Zheng, Jun Liu, Xiaozhi Zinc deficiency induces abnormal development of the myocardium by promoting SENP5 overexpression |
title | Zinc deficiency induces abnormal development of the myocardium by promoting SENP5 overexpression |
title_full | Zinc deficiency induces abnormal development of the myocardium by promoting SENP5 overexpression |
title_fullStr | Zinc deficiency induces abnormal development of the myocardium by promoting SENP5 overexpression |
title_full_unstemmed | Zinc deficiency induces abnormal development of the myocardium by promoting SENP5 overexpression |
title_short | Zinc deficiency induces abnormal development of the myocardium by promoting SENP5 overexpression |
title_sort | zinc deficiency induces abnormal development of the myocardium by promoting senp5 overexpression |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7676719/ https://www.ncbi.nlm.nih.gov/pubmed/33211757 http://dx.doi.org/10.1371/journal.pone.0242606 |
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