Mitochondrial Oxidative Stress Induces Cardiac Fibrosis in Obese Rats through Modulation of Transthyretin

A proteomic approach was used to characterize potential mediators involved in the improvement in cardiac fibrosis observed with the administration of the mitochondrial antioxidant MitoQ in obese rats. Male Wistar rats were fed a standard diet (3.5% fat; CT) or a high-fat diet (35% fat; HFD) and trea...

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Detalles Bibliográficos
Autores: Martínez Martínez, Ernesto, Fernández-Irigoyen, Joaquín, Santamaría, Enrique, Nieto, María Luisa, Bravo San Pedro, José Manuel, Cachofeiro Ramos, María Victoria
Tipo de recurso: artículo
Fecha de publicación:2022
País:España
Institución:Universidad Complutense de Madrid (UCM)
Repositorio:Docta Complutense
Idioma:inglés
OAI Identifier:oai:docta.ucm.es:20.500.14352/115423
Acceso en línea:https://hdl.handle.net/20.500.14352/115423
Access Level:acceso abierto
Palabra clave:616-056.25
endoplasmic reticulum stress
fibrosis
mitochondrial oxidative stress
obesity
transthyretin
Ciencias Biomédicas
32 Ciencias Médicas
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repository_id_str
spelling Mitochondrial Oxidative Stress Induces Cardiac Fibrosis in Obese Rats through Modulation of TransthyretinMartínez Martínez, ErnestoFernández-Irigoyen, JoaquínSantamaría, EnriqueNieto, María LuisaBravo San Pedro, José ManuelCachofeiro Ramos, María Victoria616-056.25endoplasmic reticulum stressfibrosismitochondrial oxidative stressobesitytransthyretinCiencias Biomédicas32 Ciencias MédicasA proteomic approach was used to characterize potential mediators involved in the improvement in cardiac fibrosis observed with the administration of the mitochondrial antioxidant MitoQ in obese rats. Male Wistar rats were fed a standard diet (3.5% fat; CT) or a high-fat diet (35% fat; HFD) and treated with vehicle or MitoQ (200 µM) in drinking water for 7 weeks. Obesity modulated the expression of 33 proteins as compared with controls of the more than 1000 proteins identified. These include proteins related to endoplasmic reticulum (ER) stress and oxidative stress. Proteomic analyses revealed that HFD animals presented with an increase in cardiac transthyretin (TTR) protein levels, an effect that was prevented by MitoQ treatment in obese animals. This was confirmed by plasma levels, which were associated with those of cardiac levels of both binding immunoglobulin protein (BiP), a marker of ER stress, and fibrosis. TTR stimulated collagen I production and BiP in cardiac fibroblasts. This upregulation was prevented by the presence of MitoQ. In summary, the results suggest a role of TTR in cardiac fibrosis development associated with obesity and the beneficial effects of treatment with mitochondrial antioxidants.MDPIUniversidad Complutense de Madrid20222022-01-0120222022-01-01journal articlehttp://purl.org/coar/resource_type/c_6501VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttps://hdl.handle.net/20.500.14352/115423reponame:Docta Complutenseinstname:Universidad Complutense de Madrid (UCM)Inglésengopen accesshttp://purl.org/coar/access_right/c_abf2Attribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccessoai:docta.ucm.es:20.500.14352/1154232026-06-02T12:44:21Z
dc.title.none.fl_str_mv Mitochondrial Oxidative Stress Induces Cardiac Fibrosis in Obese Rats through Modulation of Transthyretin
title Mitochondrial Oxidative Stress Induces Cardiac Fibrosis in Obese Rats through Modulation of Transthyretin
spellingShingle Mitochondrial Oxidative Stress Induces Cardiac Fibrosis in Obese Rats through Modulation of Transthyretin
Martínez Martínez, Ernesto
616-056.25
endoplasmic reticulum stress
fibrosis
mitochondrial oxidative stress
obesity
transthyretin
Ciencias Biomédicas
32 Ciencias Médicas
title_short Mitochondrial Oxidative Stress Induces Cardiac Fibrosis in Obese Rats through Modulation of Transthyretin
title_full Mitochondrial Oxidative Stress Induces Cardiac Fibrosis in Obese Rats through Modulation of Transthyretin
title_fullStr Mitochondrial Oxidative Stress Induces Cardiac Fibrosis in Obese Rats through Modulation of Transthyretin
title_full_unstemmed Mitochondrial Oxidative Stress Induces Cardiac Fibrosis in Obese Rats through Modulation of Transthyretin
title_sort Mitochondrial Oxidative Stress Induces Cardiac Fibrosis in Obese Rats through Modulation of Transthyretin
dc.creator.none.fl_str_mv Martínez Martínez, Ernesto
Fernández-Irigoyen, Joaquín
Santamaría, Enrique
Nieto, María Luisa
Bravo San Pedro, José Manuel
Cachofeiro Ramos, María Victoria
author Martínez Martínez, Ernesto
author_facet Martínez Martínez, Ernesto
Fernández-Irigoyen, Joaquín
Santamaría, Enrique
Nieto, María Luisa
Bravo San Pedro, José Manuel
Cachofeiro Ramos, María Victoria
author_role author
author2 Fernández-Irigoyen, Joaquín
Santamaría, Enrique
Nieto, María Luisa
Bravo San Pedro, José Manuel
Cachofeiro Ramos, María Victoria
author2_role author
author
author
author
author
dc.contributor.none.fl_str_mv Universidad Complutense de Madrid
dc.subject.none.fl_str_mv 616-056.25
endoplasmic reticulum stress
fibrosis
mitochondrial oxidative stress
obesity
transthyretin
Ciencias Biomédicas
32 Ciencias Médicas
topic 616-056.25
endoplasmic reticulum stress
fibrosis
mitochondrial oxidative stress
obesity
transthyretin
Ciencias Biomédicas
32 Ciencias Médicas
description A proteomic approach was used to characterize potential mediators involved in the improvement in cardiac fibrosis observed with the administration of the mitochondrial antioxidant MitoQ in obese rats. Male Wistar rats were fed a standard diet (3.5% fat; CT) or a high-fat diet (35% fat; HFD) and treated with vehicle or MitoQ (200 µM) in drinking water for 7 weeks. Obesity modulated the expression of 33 proteins as compared with controls of the more than 1000 proteins identified. These include proteins related to endoplasmic reticulum (ER) stress and oxidative stress. Proteomic analyses revealed that HFD animals presented with an increase in cardiac transthyretin (TTR) protein levels, an effect that was prevented by MitoQ treatment in obese animals. This was confirmed by plasma levels, which were associated with those of cardiac levels of both binding immunoglobulin protein (BiP), a marker of ER stress, and fibrosis. TTR stimulated collagen I production and BiP in cardiac fibroblasts. This upregulation was prevented by the presence of MitoQ. In summary, the results suggest a role of TTR in cardiac fibrosis development associated with obesity and the beneficial effects of treatment with mitochondrial antioxidants.
publishDate 2022
dc.date.none.fl_str_mv 2022
2022-01-01
2022
2022-01-01
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://hdl.handle.net/20.500.14352/115423
url https://hdl.handle.net/20.500.14352/115423
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
Attribution-NonCommercial-NoDerivatives 4.0 International
http://creativecommons.org/licenses/by-nc-nd/4.0/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
Attribution-NonCommercial-NoDerivatives 4.0 International
http://creativecommons.org/licenses/by-nc-nd/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv MDPI
publisher.none.fl_str_mv MDPI
dc.source.none.fl_str_mv reponame:Docta Complutense
instname:Universidad Complutense de Madrid (UCM)
instname_str Universidad Complutense de Madrid (UCM)
reponame_str Docta Complutense
collection Docta Complutense
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,812429

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