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Proteomic analysis of neonatal mouse hearts shows PKA functions as a cardiomyocyte replication regulator
The ability of the adult mammalian heart to regenerate can save the cardiac muscle from a loss of function caused by injury. Cardiomyocyte regeneration is a key aspect of research for the treatment of cardiovascular diseases. The mouse heart shows temporary regeneration in the first week after birth...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10566114/ https://www.ncbi.nlm.nih.gov/pubmed/37821903 http://dx.doi.org/10.1186/s12953-023-00219-4 |
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author | Hu, Lizhi Liang, Minglu Jiang, Qin Jie, Youming Chen, Long Zhang, Fengxiao |
author_facet | Hu, Lizhi Liang, Minglu Jiang, Qin Jie, Youming Chen, Long Zhang, Fengxiao |
author_sort | Hu, Lizhi |
collection | PubMed |
description | The ability of the adult mammalian heart to regenerate can save the cardiac muscle from a loss of function caused by injury. Cardiomyocyte regeneration is a key aspect of research for the treatment of cardiovascular diseases. The mouse heart shows temporary regeneration in the first week after birth; thus, the newborn mouse heart is an ideal model to study heart muscle regeneration. In this study, proteomic analysis was used to investigate the differences in protein expression in the hearts of neonatal mice at days 1 (P1 group), 4 (P4 group), and 7 (P7 group). Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis showed changes in several groups of proteins, including the protein kinase A (PKA) signaling pathway. Moreover, it was found that PKA inhibitors and agonists regulated cardiomyocyte replication in neonatal mouse hearts. These findings suggest that PKA may be a target for the regulation of the cardiomyocyte cell cycle. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12953-023-00219-4. |
format | Online Article Text |
id | pubmed-10566114 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-105661142023-10-12 Proteomic analysis of neonatal mouse hearts shows PKA functions as a cardiomyocyte replication regulator Hu, Lizhi Liang, Minglu Jiang, Qin Jie, Youming Chen, Long Zhang, Fengxiao Proteome Sci Research The ability of the adult mammalian heart to regenerate can save the cardiac muscle from a loss of function caused by injury. Cardiomyocyte regeneration is a key aspect of research for the treatment of cardiovascular diseases. The mouse heart shows temporary regeneration in the first week after birth; thus, the newborn mouse heart is an ideal model to study heart muscle regeneration. In this study, proteomic analysis was used to investigate the differences in protein expression in the hearts of neonatal mice at days 1 (P1 group), 4 (P4 group), and 7 (P7 group). Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis showed changes in several groups of proteins, including the protein kinase A (PKA) signaling pathway. Moreover, it was found that PKA inhibitors and agonists regulated cardiomyocyte replication in neonatal mouse hearts. These findings suggest that PKA may be a target for the regulation of the cardiomyocyte cell cycle. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12953-023-00219-4. BioMed Central 2023-10-11 /pmc/articles/PMC10566114/ /pubmed/37821903 http://dx.doi.org/10.1186/s12953-023-00219-4 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Hu, Lizhi Liang, Minglu Jiang, Qin Jie, Youming Chen, Long Zhang, Fengxiao Proteomic analysis of neonatal mouse hearts shows PKA functions as a cardiomyocyte replication regulator |
title | Proteomic analysis of neonatal mouse hearts shows PKA functions as a cardiomyocyte replication regulator |
title_full | Proteomic analysis of neonatal mouse hearts shows PKA functions as a cardiomyocyte replication regulator |
title_fullStr | Proteomic analysis of neonatal mouse hearts shows PKA functions as a cardiomyocyte replication regulator |
title_full_unstemmed | Proteomic analysis of neonatal mouse hearts shows PKA functions as a cardiomyocyte replication regulator |
title_short | Proteomic analysis of neonatal mouse hearts shows PKA functions as a cardiomyocyte replication regulator |
title_sort | proteomic analysis of neonatal mouse hearts shows pka functions as a cardiomyocyte replication regulator |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10566114/ https://www.ncbi.nlm.nih.gov/pubmed/37821903 http://dx.doi.org/10.1186/s12953-023-00219-4 |
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