Heart remodeling produced by aortic stenosis promotes cardiomyocyte apoptosis mediated by collagen V imbalance
Autor(a) principal: | |
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Data de Publicação: | 2018 |
Outros Autores: | , , , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
DOI: | 10.1016/j.pathophys.2018.07.001 |
Texto Completo: | http://dx.doi.org/10.1016/j.pathophys.2018.07.001 http://hdl.handle.net/11449/228560 |
Resumo: | Cardiac remodeling (CR) is a structural change of the heart due to chronic hemodynamic overload related to changes in both myocyte and extracellular matrix (ECM). We investigated that the imbalance of collagen V promotes cardiomyocyte apoptosis that contributes to heart failure and cell death. Aortic stenosis was induced surgically and male Wistar rats were randomized to 18 weeks (Sham 18 w, n = 12; AoS 18 w, n = 12) and severe of heart failure (Sham HF, n = 12; AoS HF, n = 12) groups. Functional and structural echocardiogram, immunohistochemistry for Ki-67, TUNEL assay and Immunofluorescence for collagen were performed. Our main results were: (1) Progressive reduction of cardiac functional capacity due to cardiac remodeling with decreased eject fraction in heart failure; (2) Imbalance of collagen deposition with increased, crowded and irregular collagen I in situ expression; (3) Dysregulation of dynamic control of collagen fibers with exposed epitopes of collagen V; (4) Additional apoptosis that are dependent to cardiac injury. The collagen V expression in cardiac remodeling is for the first time described and may be related to additional apoptosis and autoimmune response. Our findings suggest a critical role of collagen V in cardiac remodeling to modulate and promote heart failure and death. |
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Heart remodeling produced by aortic stenosis promotes cardiomyocyte apoptosis mediated by collagen V imbalanceAortic stenosisApoptosisCardiac remodelingCollagen VCardiac remodeling (CR) is a structural change of the heart due to chronic hemodynamic overload related to changes in both myocyte and extracellular matrix (ECM). We investigated that the imbalance of collagen V promotes cardiomyocyte apoptosis that contributes to heart failure and cell death. Aortic stenosis was induced surgically and male Wistar rats were randomized to 18 weeks (Sham 18 w, n = 12; AoS 18 w, n = 12) and severe of heart failure (Sham HF, n = 12; AoS HF, n = 12) groups. Functional and structural echocardiogram, immunohistochemistry for Ki-67, TUNEL assay and Immunofluorescence for collagen were performed. Our main results were: (1) Progressive reduction of cardiac functional capacity due to cardiac remodeling with decreased eject fraction in heart failure; (2) Imbalance of collagen deposition with increased, crowded and irregular collagen I in situ expression; (3) Dysregulation of dynamic control of collagen fibers with exposed epitopes of collagen V; (4) Additional apoptosis that are dependent to cardiac injury. The collagen V expression in cardiac remodeling is for the first time described and may be related to additional apoptosis and autoimmune response. Our findings suggest a critical role of collagen V in cardiac remodeling to modulate and promote heart failure and death.Department of Internal Medicine Botucatu Medical School São Paulo State UniversityDepartment of Pathology and Legal Medicine Ribeirão Preto Medical School University of São PauloDepartment of Pathology Faculty of Medicine University of São PauloDepartment of Internal Medicine Botucatu Medical School São Paulo State UniversityUniversidade Estadual Paulista (UNESP)Universidade de São Paulo (USP)Sant'Ana, Paula Grippa [UNESP]Batah, Sabrina SetembreLeão, Patrícia SantosTeodoro, Walcy Rosoliade Souza, Sérgio Luiz Borges [UNESP]Ferreira Mota, Gustavo Augusto [UNESP]Vileigas, Danielle Fernandes [UNESP]da Silva, Vitor Loureiro [UNESP]de Campos, Dijon Henrique Salomé [UNESP]Okoshi, Katashi [UNESP]Capelozzi, Vera LuizaCicogna, Antonio Carlos [UNESP]Fabro, Alexandre Todorovic2022-04-29T08:27:23Z2022-04-29T08:27:23Z2018-12-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article373-379http://dx.doi.org/10.1016/j.pathophys.2018.07.001Pathophysiology, v. 25, n. 4, p. 373-379, 2018.1873-149X0928-4680http://hdl.handle.net/11449/22856010.1016/j.pathophys.2018.07.0012-s2.0-85049876520Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengPathophysiologyinfo:eu-repo/semantics/openAccess2024-08-14T17:23:34Zoai:repositorio.unesp.br:11449/228560Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-14T17:23:34Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Heart remodeling produced by aortic stenosis promotes cardiomyocyte apoptosis mediated by collagen V imbalance |
title |
Heart remodeling produced by aortic stenosis promotes cardiomyocyte apoptosis mediated by collagen V imbalance |
spellingShingle |
Heart remodeling produced by aortic stenosis promotes cardiomyocyte apoptosis mediated by collagen V imbalance Heart remodeling produced by aortic stenosis promotes cardiomyocyte apoptosis mediated by collagen V imbalance Sant'Ana, Paula Grippa [UNESP] Aortic stenosis Apoptosis Cardiac remodeling Collagen V Sant'Ana, Paula Grippa [UNESP] Aortic stenosis Apoptosis Cardiac remodeling Collagen V |
title_short |
Heart remodeling produced by aortic stenosis promotes cardiomyocyte apoptosis mediated by collagen V imbalance |
title_full |
Heart remodeling produced by aortic stenosis promotes cardiomyocyte apoptosis mediated by collagen V imbalance |
title_fullStr |
Heart remodeling produced by aortic stenosis promotes cardiomyocyte apoptosis mediated by collagen V imbalance Heart remodeling produced by aortic stenosis promotes cardiomyocyte apoptosis mediated by collagen V imbalance |
title_full_unstemmed |
Heart remodeling produced by aortic stenosis promotes cardiomyocyte apoptosis mediated by collagen V imbalance Heart remodeling produced by aortic stenosis promotes cardiomyocyte apoptosis mediated by collagen V imbalance |
title_sort |
Heart remodeling produced by aortic stenosis promotes cardiomyocyte apoptosis mediated by collagen V imbalance |
author |
Sant'Ana, Paula Grippa [UNESP] |
author_facet |
Sant'Ana, Paula Grippa [UNESP] Sant'Ana, Paula Grippa [UNESP] Batah, Sabrina Setembre Leão, Patrícia Santos Teodoro, Walcy Rosolia de Souza, Sérgio Luiz Borges [UNESP] Ferreira Mota, Gustavo Augusto [UNESP] Vileigas, Danielle Fernandes [UNESP] da Silva, Vitor Loureiro [UNESP] de Campos, Dijon Henrique Salomé [UNESP] Okoshi, Katashi [UNESP] Capelozzi, Vera Luiza Cicogna, Antonio Carlos [UNESP] Fabro, Alexandre Todorovic Batah, Sabrina Setembre Leão, Patrícia Santos Teodoro, Walcy Rosolia de Souza, Sérgio Luiz Borges [UNESP] Ferreira Mota, Gustavo Augusto [UNESP] Vileigas, Danielle Fernandes [UNESP] da Silva, Vitor Loureiro [UNESP] de Campos, Dijon Henrique Salomé [UNESP] Okoshi, Katashi [UNESP] Capelozzi, Vera Luiza Cicogna, Antonio Carlos [UNESP] Fabro, Alexandre Todorovic |
author_role |
author |
author2 |
Batah, Sabrina Setembre Leão, Patrícia Santos Teodoro, Walcy Rosolia de Souza, Sérgio Luiz Borges [UNESP] Ferreira Mota, Gustavo Augusto [UNESP] Vileigas, Danielle Fernandes [UNESP] da Silva, Vitor Loureiro [UNESP] de Campos, Dijon Henrique Salomé [UNESP] Okoshi, Katashi [UNESP] Capelozzi, Vera Luiza Cicogna, Antonio Carlos [UNESP] Fabro, Alexandre Todorovic |
author2_role |
author author author author author author author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade Estadual Paulista (UNESP) Universidade de São Paulo (USP) |
dc.contributor.author.fl_str_mv |
Sant'Ana, Paula Grippa [UNESP] Batah, Sabrina Setembre Leão, Patrícia Santos Teodoro, Walcy Rosolia de Souza, Sérgio Luiz Borges [UNESP] Ferreira Mota, Gustavo Augusto [UNESP] Vileigas, Danielle Fernandes [UNESP] da Silva, Vitor Loureiro [UNESP] de Campos, Dijon Henrique Salomé [UNESP] Okoshi, Katashi [UNESP] Capelozzi, Vera Luiza Cicogna, Antonio Carlos [UNESP] Fabro, Alexandre Todorovic |
dc.subject.por.fl_str_mv |
Aortic stenosis Apoptosis Cardiac remodeling Collagen V |
topic |
Aortic stenosis Apoptosis Cardiac remodeling Collagen V |
description |
Cardiac remodeling (CR) is a structural change of the heart due to chronic hemodynamic overload related to changes in both myocyte and extracellular matrix (ECM). We investigated that the imbalance of collagen V promotes cardiomyocyte apoptosis that contributes to heart failure and cell death. Aortic stenosis was induced surgically and male Wistar rats were randomized to 18 weeks (Sham 18 w, n = 12; AoS 18 w, n = 12) and severe of heart failure (Sham HF, n = 12; AoS HF, n = 12) groups. Functional and structural echocardiogram, immunohistochemistry for Ki-67, TUNEL assay and Immunofluorescence for collagen were performed. Our main results were: (1) Progressive reduction of cardiac functional capacity due to cardiac remodeling with decreased eject fraction in heart failure; (2) Imbalance of collagen deposition with increased, crowded and irregular collagen I in situ expression; (3) Dysregulation of dynamic control of collagen fibers with exposed epitopes of collagen V; (4) Additional apoptosis that are dependent to cardiac injury. The collagen V expression in cardiac remodeling is for the first time described and may be related to additional apoptosis and autoimmune response. Our findings suggest a critical role of collagen V in cardiac remodeling to modulate and promote heart failure and death. |
publishDate |
2018 |
dc.date.none.fl_str_mv |
2018-12-01 2022-04-29T08:27:23Z 2022-04-29T08:27:23Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1016/j.pathophys.2018.07.001 Pathophysiology, v. 25, n. 4, p. 373-379, 2018. 1873-149X 0928-4680 http://hdl.handle.net/11449/228560 10.1016/j.pathophys.2018.07.001 2-s2.0-85049876520 |
url |
http://dx.doi.org/10.1016/j.pathophys.2018.07.001 http://hdl.handle.net/11449/228560 |
identifier_str_mv |
Pathophysiology, v. 25, n. 4, p. 373-379, 2018. 1873-149X 0928-4680 10.1016/j.pathophys.2018.07.001 2-s2.0-85049876520 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Pathophysiology |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
373-379 |
dc.source.none.fl_str_mv |
Scopus reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
|
_version_ |
1822231966420828160 |
dc.identifier.doi.none.fl_str_mv |
10.1016/j.pathophys.2018.07.001 |