Cardiomyocyte specific deletion of Crif1 causes mitochondrial cardiomyopathy in mice

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

doi:10.1371/journal.pone.0053577

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Cardiomyocyte specific deletion of Crif1 causes mitochondrial cardiomyopathy in mice

Journal article

Open access

Peer reviewed

Cardiomyocyte specific deletion of Crif1 causes mitochondrial cardiomyopathy in mice

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, …

PloS one, Vol.8(1), pp.e53577-e53577

2013

DOI: 10.1371/journal.pone.0053577

PMID: 23308255

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Abstract

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.

Mitochondria, Heart - ultrastructure

Mitochondria, Heart - metabolism

Adenosine Triphosphate - biosynthesis

Cardiomyopathies - genetics

Cell Respiration

Gene Deletion

Myocardium - metabolism

Cell Cycle Proteins - genetics

Integrases - metabolism

Mitochondria, Heart - genetics

Oxygen Consumption

Cardiomyopathies - pathology

Cell Cycle Proteins - deficiency

Heart Failure - genetics

Mice, Transgenic

Myocardium - pathology

Heart Failure - metabolism

Heart Failure - pathology

Tamoxifen

Myocytes, Cardiac - pathology

Animals

Cardiomyopathies - metabolism

Myocytes, Cardiac - metabolism

Mice

Integrases - genetics

Crosses, Genetic

Details

Title: Subtitle: Cardiomyocyte specific deletion of Crif1 causes mitochondrial cardiomyopathy in mice
Creators: Juhee Shin - Department of Biological Sciences, Seoul National University, Gwanak-gu, Seoul, Republic of Korea
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
Resource Type: Journal article
Publication Details: PloS one, Vol.8(1), pp.e53577-e53577
DOI: 10.1371/journal.pone.0053577
PMID: 23308255
NLM abbreviation: PLoS One
ISSN: 1932-6203
eISSN: 1932-6203
Publisher: Public Library of Science; United States
Language: English
Date published: 2013
Academic Unit: Roy J. Carver Department of Biomedical Engineering; Fraternal Order of Eagles Diabetes Research Center; Biochemistry and Molecular Biology; Endocrinology and Metabolism; Internal Medicine
Record Identifier: 9984024511702771

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