Cardiomyocyte specific deletion of Crif1 causes mitochondrial cardiomyopathy in mice.
Mitochondria are key organelles dedicated to energy production. Crif1, which interacts with the large subunit of the mitochondrial ribosome, is indispensable for the mitochondrial translation and membrane insertion of respiratory subunits. To explore the physiological function of Crif1 in the heart,...
| Main Authors: | , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2013-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3537664?pdf=render |
| _version_ | 1819171685518016512 |
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| author | Juhee Shin Seok Hong Lee Min-Chul Kwon Dong Kwon Yang Ha-Rim Seo Jaetaek Kim Yoon-Young Kim Sun-Kyoung Im Evan Dale Abel Kyong-Tai Kim Woo Jin Park Young-Yun Kong |
| author_facet | Juhee Shin Seok Hong Lee Min-Chul Kwon Dong Kwon Yang Ha-Rim Seo Jaetaek Kim Yoon-Young Kim Sun-Kyoung Im Evan Dale Abel Kyong-Tai Kim Woo Jin Park Young-Yun Kong |
| author_sort | Juhee Shin |
| collection | DOAJ |
| description | Mitochondria are key organelles dedicated to energy production. Crif1, which interacts with the large subunit of the mitochondrial ribosome, is indispensable for the mitochondrial translation and membrane insertion of respiratory subunits. To explore the physiological function of Crif1 in the heart, Crif1(f/f) mice were crossed with Myh6-cre/Esr1 transgenic mice, which harbor cardiomyocyte-specific Cre activity in a tamoxifen-dependent manner. The tamoxifen injections were given at six weeks postnatal, and the mutant mice survived only five months due to hypertrophic heart failure. In the mutant cardiac muscles, mitochondrial mass dramatically increased, while the inner structure was altered with lack of cristae. Mutant cardiac muscles showed decreased rates of oxygen consumption and ATP production, suggesting that Crif1 plays a critical role in the maintenance of both mitochondrial structure and respiration in cardiac muscles. |
| first_indexed | 2024-12-22T19:55:13Z |
| format | Article |
| id | doaj.art-4c8cbf04b21246659ad8b30804500836 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-22T19:55:13Z |
| publishDate | 2013-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-4c8cbf04b21246659ad8b308045008362022-12-21T18:14:26ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-0181e5357710.1371/journal.pone.0053577Cardiomyocyte specific deletion of Crif1 causes mitochondrial cardiomyopathy in mice.Juhee ShinSeok Hong LeeMin-Chul KwonDong Kwon YangHa-Rim SeoJaetaek KimYoon-Young KimSun-Kyoung ImEvan Dale AbelKyong-Tai KimWoo Jin ParkYoung-Yun KongMitochondria are key organelles dedicated to energy production. Crif1, which interacts with the large subunit of the mitochondrial ribosome, is indispensable for the mitochondrial translation and membrane insertion of respiratory subunits. To explore the physiological function of Crif1 in the heart, Crif1(f/f) mice were crossed with Myh6-cre/Esr1 transgenic mice, which harbor cardiomyocyte-specific Cre activity in a tamoxifen-dependent manner. The tamoxifen injections were given at six weeks postnatal, and the mutant mice survived only five months due to hypertrophic heart failure. In the mutant cardiac muscles, mitochondrial mass dramatically increased, while the inner structure was altered with lack of cristae. Mutant cardiac muscles showed decreased rates of oxygen consumption and ATP production, suggesting that Crif1 plays a critical role in the maintenance of both mitochondrial structure and respiration in cardiac muscles.http://europepmc.org/articles/PMC3537664?pdf=render |
| spellingShingle | Juhee Shin Seok Hong Lee Min-Chul Kwon Dong Kwon Yang Ha-Rim Seo Jaetaek Kim Yoon-Young Kim Sun-Kyoung Im Evan Dale Abel Kyong-Tai Kim Woo Jin Park Young-Yun Kong Cardiomyocyte specific deletion of Crif1 causes mitochondrial cardiomyopathy in mice. PLoS ONE |
| title | Cardiomyocyte specific deletion of Crif1 causes mitochondrial cardiomyopathy in mice. |
| title_full | Cardiomyocyte specific deletion of Crif1 causes mitochondrial cardiomyopathy in mice. |
| title_fullStr | Cardiomyocyte specific deletion of Crif1 causes mitochondrial cardiomyopathy in mice. |
| title_full_unstemmed | Cardiomyocyte specific deletion of Crif1 causes mitochondrial cardiomyopathy in mice. |
| title_short | Cardiomyocyte specific deletion of Crif1 causes mitochondrial cardiomyopathy in mice. |
| title_sort | cardiomyocyte specific deletion of crif1 causes mitochondrial cardiomyopathy in mice |
| url | http://europepmc.org/articles/PMC3537664?pdf=render |
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