Omentin protects H9c2 cells against docetaxel cardiotoxicity

Background : Association between obesity and cardiovascular diseases is well known, however increased susceptibility of obese patients to develop several cancer types is not so commonly known. Current data suggest that poorer overall survival in cancer patients might be associated to non-cancer-rela...

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Autores: Lage Fernández, Ricardo, Cebro Márquez, María, Rodríguez Mañero, Moisés, González Juanatey, José Ramón, Moscoso Galán, Isabel
Tipo de recurso: artículo
Fecha de publicación:2019
País:España
Institución:Universidad de Santiago de Compostela (USC)
Repositorio:Minerva. Repositorio Institucional de la Universidad de Santiago de Compostela
Idioma:inglés
OAI Identifier:oai:minerva.usc.gal:10347/21081
Acceso en línea:http://hdl.handle.net/10347/21081
Access Level:acceso abierto
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spelling Omentin protects H9c2 cells against docetaxel cardiotoxicityLage Fernández, RicardoCebro Márquez, MaríaRodríguez Mañero, MoisésGonzález Juanatey, José RamónMoscoso Galán, IsabelBackground : Association between obesity and cardiovascular diseases is well known, however increased susceptibility of obese patients to develop several cancer types is not so commonly known. Current data suggest that poorer overall survival in cancer patients might be associated to non-cancer-related causes such as higher risk of cardiotoxicity in obese patients treated with chemotherapeutic agents. Omentin, a novel adipokine decreased in obesity, is actually in the spotlight due to its favourable effects on inflammation, glucose homeostasis and cardiovascular diseases. Also, recent data showed that in vitro anthracycline-induced cardiomyocyte apoptosis is counteracted by omentin suggesting its cardioprotective role. Objective: Our aim was to evaluate omentin effects against docetaxel toxicity. Results: Our data indicate that omentin inhibits docetaxel-induced viability loss and that increased viability is associated to decreased caspase-3 expression and cell death. Although omentin reduces NOX4 expression, it failed to reduce docetaxel-induced reactive oxygen species production. Our results indicate that omentin decreases docetaxel-induced endoplasmic reticulum stress, suggesting that cardioprotective role might be associated to ERS inhibition. Conclusion : These data suggest that omentin treatment may contribute to decrease susceptibility to DTX-induced cardiotoxicity.PLOSUniversidade de Santiago de Compostela. Centro de Investigación en Medicina Molecular e Enfermidades CrónicasUniversidade de Santiago de Compostela. Departamento de Psiquiatría, Radioloxía, Saúde Pública, Enfermaría e Medicina20192019-01-0120192019-01-01journal articlehttp://purl.org/coar/resource_type/c_6501VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/10347/21081reponame:Minerva. Repositorio Institucional de la Universidad de Santiago de Compostelainstname:Universidad de Santiago de Compostela (USC)Inglésengopen accesshttp://purl.org/coar/access_right/c_abf2© 2019 Lage et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.https://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:minerva.usc.gal:10347/210812026-06-15T12:47:27Z
dc.title.none.fl_str_mv Omentin protects H9c2 cells against docetaxel cardiotoxicity
title Omentin protects H9c2 cells against docetaxel cardiotoxicity
spellingShingle Omentin protects H9c2 cells against docetaxel cardiotoxicity
Lage Fernández, Ricardo
title_short Omentin protects H9c2 cells against docetaxel cardiotoxicity
title_full Omentin protects H9c2 cells against docetaxel cardiotoxicity
title_fullStr Omentin protects H9c2 cells against docetaxel cardiotoxicity
title_full_unstemmed Omentin protects H9c2 cells against docetaxel cardiotoxicity
title_sort Omentin protects H9c2 cells against docetaxel cardiotoxicity
dc.creator.none.fl_str_mv Lage Fernández, Ricardo
Cebro Márquez, María
Rodríguez Mañero, Moisés
González Juanatey, José Ramón
Moscoso Galán, Isabel
author Lage Fernández, Ricardo
author_facet Lage Fernández, Ricardo
Cebro Márquez, María
Rodríguez Mañero, Moisés
González Juanatey, José Ramón
Moscoso Galán, Isabel
author_role author
author2 Cebro Márquez, María
Rodríguez Mañero, Moisés
González Juanatey, José Ramón
Moscoso Galán, Isabel
author2_role author
author
author
author
dc.contributor.none.fl_str_mv Universidade de Santiago de Compostela. Centro de Investigación en Medicina Molecular e Enfermidades Crónicas
Universidade de Santiago de Compostela. Departamento de Psiquiatría, Radioloxía, Saúde Pública, Enfermaría e Medicina
description Background : Association between obesity and cardiovascular diseases is well known, however increased susceptibility of obese patients to develop several cancer types is not so commonly known. Current data suggest that poorer overall survival in cancer patients might be associated to non-cancer-related causes such as higher risk of cardiotoxicity in obese patients treated with chemotherapeutic agents. Omentin, a novel adipokine decreased in obesity, is actually in the spotlight due to its favourable effects on inflammation, glucose homeostasis and cardiovascular diseases. Also, recent data showed that in vitro anthracycline-induced cardiomyocyte apoptosis is counteracted by omentin suggesting its cardioprotective role. Objective: Our aim was to evaluate omentin effects against docetaxel toxicity. Results: Our data indicate that omentin inhibits docetaxel-induced viability loss and that increased viability is associated to decreased caspase-3 expression and cell death. Although omentin reduces NOX4 expression, it failed to reduce docetaxel-induced reactive oxygen species production. Our results indicate that omentin decreases docetaxel-induced endoplasmic reticulum stress, suggesting that cardioprotective role might be associated to ERS inhibition. Conclusion : These data suggest that omentin treatment may contribute to decrease susceptibility to DTX-induced cardiotoxicity.
publishDate 2019
dc.date.none.fl_str_mv 2019
2019-01-01
2019
2019-01-01
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 http://hdl.handle.net/10347/21081
url http://hdl.handle.net/10347/21081
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
https://creativecommons.org/licenses/by/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
https://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv PLOS
publisher.none.fl_str_mv PLOS
dc.source.none.fl_str_mv reponame:Minerva. Repositorio Institucional de la Universidad de Santiago de Compostela
instname:Universidad de Santiago de Compostela (USC)
instname_str Universidad de Santiago de Compostela (USC)
reponame_str Minerva. Repositorio Institucional de la Universidad de Santiago de Compostela
collection Minerva. Repositorio Institucional de la Universidad de Santiago de Compostela
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