Coenzyme Q deficiency triggers mitochondria degradation by mitophagy

Coenzyme Q(10) (CoQ) is a small lipophilic molecule critical for the transport of electrons from complexes I and II to complex III in the mitochondrial respiratory chain. CoQ deficiency is a rare human genetic condition that has been associated with a variety of clinical phenotypes. With the aim of...

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Autores: Rodríguez-Hernández A, Cordero MD, Salviati L, Artuch R, Pineda M, Briones P, Gómez Izquierdo L, Cotán D, Navas P, Sánchez-Alcázar JA
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2009
País:España
Institución:Fundació Sant Joan de Déu
Repositorio:r-FSJD. Repositorio Institucional de Producción Científica de la Fundació Sant Joan de Déu
OAI Identifier:oai:fsjd.fundanetsuite.com:p1444
Acceso en línea:https://fsjd.fundanetsuite.com/Publicaciones/ProdCientif/PublicacionFrw.aspx?id=1444
Access Level:acceso abierto
Palabra clave:autophagy
coenzyme Q
free radicals
mitochondria
mitochondrial disease
mitochondrial permeability transition
mitophagy
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spelling Coenzyme Q deficiency triggers mitochondria degradation by mitophagyRodríguez-Hernández ACordero MDSalviati LArtuch RPineda MBriones PGómez Izquierdo LCotán DNavas PSánchez-Alcázar JAautophagycoenzyme Qfree radicalsmitochondriamitochondrial diseasemitochondrial permeability transitionmitophagyCoenzyme Q(10) (CoQ) is a small lipophilic molecule critical for the transport of electrons from complexes I and II to complex III in the mitochondrial respiratory chain. CoQ deficiency is a rare human genetic condition that has been associated with a variety of clinical phenotypes. With the aim of elucidating how CoQ deficiency affects an organism, we have investigated the pathophysiologic processes present within fibroblasts derived from four patients with CoQ deficiency. Assays of cultured fibroblasts revealed decreased activities of complex II + III, complex III and complex TV, reduced expression of mitochondrial proteins involved in oxidative phosphorylation, decreased mitochondrial membrane potential, increased production of reactive oxygen species (ROS), activation of mitochondrial permeability transition (MPT), and reduced growth rates. These abnormalities were partially restored by CoQ supplementation. Moreover, we demonstrate that CoQ-deficient fibroblasts exhibited increased levels of lysosomal markers (P-galactosidase, cathepsin, LC3 and Lyso Tracker), and enhanced expression of autophagic genes at both transcriptional and translational levels, indicating the presence of autophagy. Electron microscopy studies confirmed a massive degradation of the altered mitochondria by mitophagy. Autophagy in CoQ-deficient fibroblasts was abolished by antioxidants or cyclosporin treatments suggesting that both ROS and MPT participate in this process. Furthermore, prevention of autophagy in CoQ-deficient fibroblasts by 3-methyl adenine or wortmannin, as well as the induction of CoQ deficiency in cells lacking autophagy (by means of genetic knockout of the Atg5 gene in mouse embryonic fibroblasts) resulted in apoptotic cell death, suggesting a protective role of autophagy in CoQ deficiency.TAYLOR & FRANCIS INC2009info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttps://fsjd.fundanetsuite.com/Publicaciones/ProdCientif/PublicacionFrw.aspx?id=1444AutophagyISSN: 15548627ISSNe: 15548635reponame:r-FSJD. Repositorio Institucional de Producción Científica de la Fundació Sant Joan de Déuinstname:Fundació Sant Joan de DéuInglésinfo:eu-repo/semantics/openAccessoai:fsjd.fundanetsuite.com:p14442026-05-27T12:37:41Z
dc.title.none.fl_str_mv Coenzyme Q deficiency triggers mitochondria degradation by mitophagy
title Coenzyme Q deficiency triggers mitochondria degradation by mitophagy
spellingShingle Coenzyme Q deficiency triggers mitochondria degradation by mitophagy
Rodríguez-Hernández A
autophagy
coenzyme Q
free radicals
mitochondria
mitochondrial disease
mitochondrial permeability transition
mitophagy
title_short Coenzyme Q deficiency triggers mitochondria degradation by mitophagy
title_full Coenzyme Q deficiency triggers mitochondria degradation by mitophagy
title_fullStr Coenzyme Q deficiency triggers mitochondria degradation by mitophagy
title_full_unstemmed Coenzyme Q deficiency triggers mitochondria degradation by mitophagy
title_sort Coenzyme Q deficiency triggers mitochondria degradation by mitophagy
dc.creator.none.fl_str_mv Rodríguez-Hernández A
Cordero MD
Salviati L
Artuch R
Pineda M
Briones P
Gómez Izquierdo L
Cotán D
Navas P
Sánchez-Alcázar JA
author Rodríguez-Hernández A
author_facet Rodríguez-Hernández A
Cordero MD
Salviati L
Artuch R
Pineda M
Briones P
Gómez Izquierdo L
Cotán D
Navas P
Sánchez-Alcázar JA
author_role author
author2 Cordero MD
Salviati L
Artuch R
Pineda M
Briones P
Gómez Izquierdo L
Cotán D
Navas P
Sánchez-Alcázar JA
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv autophagy
coenzyme Q
free radicals
mitochondria
mitochondrial disease
mitochondrial permeability transition
mitophagy
topic autophagy
coenzyme Q
free radicals
mitochondria
mitochondrial disease
mitochondrial permeability transition
mitophagy
description Coenzyme Q(10) (CoQ) is a small lipophilic molecule critical for the transport of electrons from complexes I and II to complex III in the mitochondrial respiratory chain. CoQ deficiency is a rare human genetic condition that has been associated with a variety of clinical phenotypes. With the aim of elucidating how CoQ deficiency affects an organism, we have investigated the pathophysiologic processes present within fibroblasts derived from four patients with CoQ deficiency. Assays of cultured fibroblasts revealed decreased activities of complex II + III, complex III and complex TV, reduced expression of mitochondrial proteins involved in oxidative phosphorylation, decreased mitochondrial membrane potential, increased production of reactive oxygen species (ROS), activation of mitochondrial permeability transition (MPT), and reduced growth rates. These abnormalities were partially restored by CoQ supplementation. Moreover, we demonstrate that CoQ-deficient fibroblasts exhibited increased levels of lysosomal markers (P-galactosidase, cathepsin, LC3 and Lyso Tracker), and enhanced expression of autophagic genes at both transcriptional and translational levels, indicating the presence of autophagy. Electron microscopy studies confirmed a massive degradation of the altered mitochondria by mitophagy. Autophagy in CoQ-deficient fibroblasts was abolished by antioxidants or cyclosporin treatments suggesting that both ROS and MPT participate in this process. Furthermore, prevention of autophagy in CoQ-deficient fibroblasts by 3-methyl adenine or wortmannin, as well as the induction of CoQ deficiency in cells lacking autophagy (by means of genetic knockout of the Atg5 gene in mouse embryonic fibroblasts) resulted in apoptotic cell death, suggesting a protective role of autophagy in CoQ deficiency.
publishDate 2009
dc.date.none.fl_str_mv 2009
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://fsjd.fundanetsuite.com/Publicaciones/ProdCientif/PublicacionFrw.aspx?id=1444
url https://fsjd.fundanetsuite.com/Publicaciones/ProdCientif/PublicacionFrw.aspx?id=1444
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.publisher.none.fl_str_mv TAYLOR & FRANCIS INC
publisher.none.fl_str_mv TAYLOR & FRANCIS INC
dc.source.none.fl_str_mv Autophagy
ISSN: 15548627
ISSNe: 15548635
reponame:r-FSJD. Repositorio Institucional de Producción Científica de la Fundació Sant Joan de Déu
instname:Fundació Sant Joan de Déu
instname_str Fundació Sant Joan de Déu
reponame_str r-FSJD. Repositorio Institucional de Producción Científica de la Fundació Sant Joan de Déu
collection r-FSJD. Repositorio Institucional de Producción Científica de la Fundació Sant Joan de Déu
repository.name.fl_str_mv
repository.mail.fl_str_mv
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