β-catenin ameliorates myocardial infarction by preventing YAP-associated apoptosis

Objective: To explore whether the effect of β-catenin on MI and MI-induced cardiomyocyte apoptosis is YAP-dependent. Methods: The authors established an MI rat model by ligating the anterior descending branch of the left coronary artery, and an MI cell model by treating cardiomyocytes with H2O2. Res...

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Detalles Bibliográficos
Autores: Kang, Haofei, Jiang, Weiwei
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2023
País:Brasil
Institución:Universidade de São Paulo (USP)
Repositorio:Clinics
Idioma:inglés
OAI Identifier:oai:revistas.usp.br:article/213767
Acceso en línea:https://www.revistas.usp.br/clinics/article/view/213767
Access Level:acceso abierto
Palabra clave:β-catenin
Cardiomyocytes
Heart failure
Myocardial Infarction
Yes-associated protein (YAP)
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repository_id_str
spelling β-catenin ameliorates myocardial infarction by preventing YAP-associated apoptosisβ-cateninCardiomyocytesHeart failureMyocardial InfarctionYes-associated protein (YAP)Objective: To explore whether the effect of β-catenin on MI and MI-induced cardiomyocyte apoptosis is YAP-dependent. Methods: The authors established an MI rat model by ligating the anterior descending branch of the left coronary artery, and an MI cell model by treating cardiomyocytes with H2O2. Results: β-catenin downregulation was observed in MI cardiac tissues and in H2O2-treated cardiomyocytes. Lentiviral-CTNNB1 was administered to MI rats to upregulate β-catenin expression in MI cardiac tissue. β-catenin recovery reduced the myocardial infarct area, fibrosis, and apoptotic cell death in MI rats. H2O2 treatment attenuated cell viability and induced cell death in cardiomyocytes, whereas β-catenin overexpression partially reversed these changes. Moreover, H2O2 treatment caused the deactivation of Yes-Associated Protein (YAP), as detected by increased YAP phosphorylation and reduced the nuclear localization of YAP. Upregulation of β-catenin expression reactivated YAP in H2O2-treated cardiomyocytes. Reactivation of YAP was achieved by administration of Mitochonic Acid-5 (MA-5) to H2O2-treated cardiomyocytes, and deactivation of YAP by CIL56 treatment in β-catenin-overexpressing H2O2-treated cardiomyocytes. MA-5 administration increased cell viability and repressed apoptosis in H2O2-treated cardiomyocytes, whereas CIL56 treatment counteracted the effects of β-catenin overexpression on cell survival and apoptosis. Conclusions: The present data indicate that β-catenin and YAP are effective treatment targets for MI, blocking the apoptotic death of cardiomyocytes.Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2023-04-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/21376710.1016/j.clinsp.2023.100189Clinics; Vol. 78 (2023); 100189Clinics; v. 78 (2023); 100189Clinics; Vol. 78 (2023); 1001891980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/213767/195926Copyright (c) 2023 Clinicsinfo:eu-repo/semantics/openAccessKang, HaofeiJiang, Weiwei2023-07-06T13:05:38Zoai:revistas.usp.br:article/213767Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2023-07-06T13:05:38Clinics - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv β-catenin ameliorates myocardial infarction by preventing YAP-associated apoptosis
title β-catenin ameliorates myocardial infarction by preventing YAP-associated apoptosis
spellingShingle β-catenin ameliorates myocardial infarction by preventing YAP-associated apoptosis
Kang, Haofei
β-catenin
Cardiomyocytes
Heart failure
Myocardial Infarction
Yes-associated protein (YAP)
title_short β-catenin ameliorates myocardial infarction by preventing YAP-associated apoptosis
title_full β-catenin ameliorates myocardial infarction by preventing YAP-associated apoptosis
title_fullStr β-catenin ameliorates myocardial infarction by preventing YAP-associated apoptosis
title_full_unstemmed β-catenin ameliorates myocardial infarction by preventing YAP-associated apoptosis
title_sort β-catenin ameliorates myocardial infarction by preventing YAP-associated apoptosis
dc.creator.none.fl_str_mv Kang, Haofei
Jiang, Weiwei
author Kang, Haofei
author_facet Kang, Haofei
Jiang, Weiwei
author_role author
author2 Jiang, Weiwei
author2_role author
dc.subject.por.fl_str_mv β-catenin
Cardiomyocytes
Heart failure
Myocardial Infarction
Yes-associated protein (YAP)
topic β-catenin
Cardiomyocytes
Heart failure
Myocardial Infarction
Yes-associated protein (YAP)
description Objective: To explore whether the effect of β-catenin on MI and MI-induced cardiomyocyte apoptosis is YAP-dependent. Methods: The authors established an MI rat model by ligating the anterior descending branch of the left coronary artery, and an MI cell model by treating cardiomyocytes with H2O2. Results: β-catenin downregulation was observed in MI cardiac tissues and in H2O2-treated cardiomyocytes. Lentiviral-CTNNB1 was administered to MI rats to upregulate β-catenin expression in MI cardiac tissue. β-catenin recovery reduced the myocardial infarct area, fibrosis, and apoptotic cell death in MI rats. H2O2 treatment attenuated cell viability and induced cell death in cardiomyocytes, whereas β-catenin overexpression partially reversed these changes. Moreover, H2O2 treatment caused the deactivation of Yes-Associated Protein (YAP), as detected by increased YAP phosphorylation and reduced the nuclear localization of YAP. Upregulation of β-catenin expression reactivated YAP in H2O2-treated cardiomyocytes. Reactivation of YAP was achieved by administration of Mitochonic Acid-5 (MA-5) to H2O2-treated cardiomyocytes, and deactivation of YAP by CIL56 treatment in β-catenin-overexpressing H2O2-treated cardiomyocytes. MA-5 administration increased cell viability and repressed apoptosis in H2O2-treated cardiomyocytes, whereas CIL56 treatment counteracted the effects of β-catenin overexpression on cell survival and apoptosis. Conclusions: The present data indicate that β-catenin and YAP are effective treatment targets for MI, blocking the apoptotic death of cardiomyocytes.
publishDate 2023
dc.date.none.fl_str_mv 2023-04-02
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/clinics/article/view/213767
10.1016/j.clinsp.2023.100189
url https://www.revistas.usp.br/clinics/article/view/213767
identifier_str_mv 10.1016/j.clinsp.2023.100189
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/clinics/article/view/213767/195926
dc.rights.driver.fl_str_mv Copyright (c) 2023 Clinics
info:eu-repo/semantics/openAccess
rights_invalid_str_mv Copyright (c) 2023 Clinics
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
dc.source.none.fl_str_mv Clinics; Vol. 78 (2023); 100189
Clinics; v. 78 (2023); 100189
Clinics; Vol. 78 (2023); 100189
1980-5322
1807-5932
reponame:Clinics
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Clinics
collection Clinics
repository.name.fl_str_mv Clinics - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||clinics@hc.fm.usp.br
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