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Neonatal Death and Heart Failure in Mouse with Transgenic HSP60 Expression
Mitochondrial heat shock proteins, such as HSP60, are chaperones responsible for the folding, transport, and quality control of mitochondrial matrix proteins and are essential for maintaining life. Both prosurvival and proapoptotic roles have been proposed for HSP60, and HSP60 is reportedly involved...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4609373/ https://www.ncbi.nlm.nih.gov/pubmed/26504810 http://dx.doi.org/10.1155/2015/539805 |
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author | Chen, Tsung-Hsien Liu, Shan-Wen Chen, Mei-Ru Cho, Kuan-Hung Chen, Tzu-Yin Chu, Pao-Hsien Kao, Yu-Ying Hsu, Ching-Han Lin, Kurt Ming-Chao |
author_facet | Chen, Tsung-Hsien Liu, Shan-Wen Chen, Mei-Ru Cho, Kuan-Hung Chen, Tzu-Yin Chu, Pao-Hsien Kao, Yu-Ying Hsu, Ching-Han Lin, Kurt Ming-Chao |
author_sort | Chen, Tsung-Hsien |
collection | PubMed |
description | Mitochondrial heat shock proteins, such as HSP60, are chaperones responsible for the folding, transport, and quality control of mitochondrial matrix proteins and are essential for maintaining life. Both prosurvival and proapoptotic roles have been proposed for HSP60, and HSP60 is reportedly involved in the initiation of autoimmune, metabolic, and cardiovascular diseases. The role of HSP60 in pathogenesis of these diseases remains unclear, partly because of the lack of mouse models expressing HSP60. In this study we generated HSP60 conditional transgenic mice suitable for investigating in vivo outcomes by expressing HSP60 at the targeted organ in disease models. Ubiquitous HSP60 induction in the embryonic stage caused neonatal death in mice at postnatal day 1. A high incidence of atrial septal defects was observed in HSP60-expressing mice, with increased apoptosis and myocyte degeneration that possibly contributed to massive hemorrhage and sponge-like cardiac muscles. Our results showed that neonatal heart failure through HSP60 induction likely involves developmental defects and excessive apoptosis. The conditional HSP60 mouse model is useful for studying crucial biological questions concerning HSP60. |
format | Online Article Text |
id | pubmed-4609373 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-46093732015-10-26 Neonatal Death and Heart Failure in Mouse with Transgenic HSP60 Expression Chen, Tsung-Hsien Liu, Shan-Wen Chen, Mei-Ru Cho, Kuan-Hung Chen, Tzu-Yin Chu, Pao-Hsien Kao, Yu-Ying Hsu, Ching-Han Lin, Kurt Ming-Chao Biomed Res Int Research Article Mitochondrial heat shock proteins, such as HSP60, are chaperones responsible for the folding, transport, and quality control of mitochondrial matrix proteins and are essential for maintaining life. Both prosurvival and proapoptotic roles have been proposed for HSP60, and HSP60 is reportedly involved in the initiation of autoimmune, metabolic, and cardiovascular diseases. The role of HSP60 in pathogenesis of these diseases remains unclear, partly because of the lack of mouse models expressing HSP60. In this study we generated HSP60 conditional transgenic mice suitable for investigating in vivo outcomes by expressing HSP60 at the targeted organ in disease models. Ubiquitous HSP60 induction in the embryonic stage caused neonatal death in mice at postnatal day 1. A high incidence of atrial septal defects was observed in HSP60-expressing mice, with increased apoptosis and myocyte degeneration that possibly contributed to massive hemorrhage and sponge-like cardiac muscles. Our results showed that neonatal heart failure through HSP60 induction likely involves developmental defects and excessive apoptosis. The conditional HSP60 mouse model is useful for studying crucial biological questions concerning HSP60. Hindawi Publishing Corporation 2015 2015-10-04 /pmc/articles/PMC4609373/ /pubmed/26504810 http://dx.doi.org/10.1155/2015/539805 Text en Copyright © 2015 Tsung-Hsien Chen et al. https://creativecommons.org/licenses/by/3.0/ 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 Chen, Tsung-Hsien Liu, Shan-Wen Chen, Mei-Ru Cho, Kuan-Hung Chen, Tzu-Yin Chu, Pao-Hsien Kao, Yu-Ying Hsu, Ching-Han Lin, Kurt Ming-Chao Neonatal Death and Heart Failure in Mouse with Transgenic HSP60 Expression |
title | Neonatal Death and Heart Failure in Mouse with Transgenic HSP60 Expression |
title_full | Neonatal Death and Heart Failure in Mouse with Transgenic HSP60 Expression |
title_fullStr | Neonatal Death and Heart Failure in Mouse with Transgenic HSP60 Expression |
title_full_unstemmed | Neonatal Death and Heart Failure in Mouse with Transgenic HSP60 Expression |
title_short | Neonatal Death and Heart Failure in Mouse with Transgenic HSP60 Expression |
title_sort | neonatal death and heart failure in mouse with transgenic hsp60 expression |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4609373/ https://www.ncbi.nlm.nih.gov/pubmed/26504810 http://dx.doi.org/10.1155/2015/539805 |
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