Stanozolol induces ventricular dysfunction by decreasing phospholamban phosphorylation in heart tissue of LDLr-/- mice

Detalhes bibliográficos
Autor(a) principal: Andrade, Tadeu Uggere de
Data de Publicação: 2022
Outros Autores: Dubois Fillho, Dionisio, Silva, Cristiane Lyrio da, Silva, Mirian de Almeida, Almeida, Simone Alves de, Nascimento, Andrews Marques do, Bissoli, Nazaré Souza, Brasil, Girlandia Alexandre, Lima, Ewelyne Miranda de
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Research, Society and Development
Texto Completo: https://rsdjournal.org/index.php/rsd/article/view/27876
Resumo: Stanozolol is a steroid that causes lipid deposition in LDLr-/- mice, although the mechanism by which this dyslipidemia results in cardiac dysfunction is little understood. The aim of this study was to evaluate the effect of stanozolol on cardiac contractility and the participation of myocardial phospholamban (pPLB) phosphorylation in an atherosclerosis mouse model. LDL receptor knockout mice (LDLr-/-) were fed a standard chow diet and received weekly subcutaneous injections of either saline (control, C group) or 20 mg/kg stanozolol (S group). After 8 weeks, hemodynamic parameters were assessed in the left ventricle. The heart was collected, weighted for hypertrophy evaluation, and kept in formalin buffer for morphometric analysis (H&E) and collagen quantification (Picrossirius). Protein expression of PLB and its phosphorylated form (p-PLB) in the left ventricle was determined by western blot. We observed that stanozolol treatment favored cardiac hypertrophy and collagen deposition in heart tissue. Also, stanozolol induced left ventricle dysfunction, increasing PBL expression and decreasing the p-PLB/PLB ratio. Altogether, our data showed that stanozolol causes cardiac remodeling and ventricular dysfunction by decreasing PLB phosphorylation in the left ventricle of LDLr-/- mice.
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spelling Stanozolol induces ventricular dysfunction by decreasing phospholamban phosphorylation in heart tissue of LDLr-/- mice El estanozolol induce disfunción ventricular al reducir la fosforilación de fosfolamban en el tejido cardíaco de ratones LDLr-/-O estanozolol induz disfunção ventricular pela redução da fosforilação do fosfolambam no tecido cardíaco de camundongos LDLr-/-Anabolic androgenic steroidsHemodynamic parametersCardiac remodelingPhospholamban phosphorylation.Esteróide anabolico androgênicoParâmetros hemodinâmicosRemodelamento cardíacoFosfolambam fosforilada.Esteroide androgénico anabólicoParámetros hemodinâmicosRemodelado cardíacoFosfolambano fosforilado.Stanozolol is a steroid that causes lipid deposition in LDLr-/- mice, although the mechanism by which this dyslipidemia results in cardiac dysfunction is little understood. The aim of this study was to evaluate the effect of stanozolol on cardiac contractility and the participation of myocardial phospholamban (pPLB) phosphorylation in an atherosclerosis mouse model. LDL receptor knockout mice (LDLr-/-) were fed a standard chow diet and received weekly subcutaneous injections of either saline (control, C group) or 20 mg/kg stanozolol (S group). After 8 weeks, hemodynamic parameters were assessed in the left ventricle. The heart was collected, weighted for hypertrophy evaluation, and kept in formalin buffer for morphometric analysis (H&E) and collagen quantification (Picrossirius). Protein expression of PLB and its phosphorylated form (p-PLB) in the left ventricle was determined by western blot. We observed that stanozolol treatment favored cardiac hypertrophy and collagen deposition in heart tissue. Also, stanozolol induced left ventricle dysfunction, increasing PBL expression and decreasing the p-PLB/PLB ratio. Altogether, our data showed that stanozolol causes cardiac remodeling and ventricular dysfunction by decreasing PLB phosphorylation in the left ventricle of LDLr-/- mice.El estanozolol es un esteroide que promueve el depósito de lípidos en las arterias de ratones LDLr-/-, sin embargo, el mecanismo por el cual la dislipidemia promueve la disfunción cardíaca en estos animales aún no se conoce bien. Por lo tanto, el objetivo del presente estudio es evaluar el efecto del estanozolol sobre la contractilidad cardíaca y la participación de la fosforilación de la proteína fosfolambano miocárdico (pPBL) en el modelo animal de aterosclerosis. Se alimentó a ratones sin receptor de LDL (LDLr-/-) con una dieta estándar de casa de animales y recibieron inyecciones subcutáneas semanales de solución salina (grupo de control, C) o 20 mg/kg de estanozolol (grupo S). Después de ocho semanas de tratamiento, se evaluaron los parámetros hemodinámicos en el ventrículo izquierdo. Luego se recolectó el corazón, se pesó para determinar la hipertrofia y se almacenó en tampón de formalina para análisis morfométrico (H&E) y cuantificación de colágeno (picrosirius). La expresión de la proteína fosfolambano (PBL) y su forma fosforilada (p-PBL) en el ventrículo izquierdo se determinó por western blot. Observamos que el tratamiento con estanozolol favorecía la hipertrofia y el depósito de colágeno en el tejido cardíaco. Además, el estanozolol indujo disfunción ventricular izquierda, aumentó la expresión de PBL y redujo la relación p-PBL/PBL. En conjunto, nuestros datos muestran que el estanozolol promueve la remodelación cardíaca y la disfunción ventricular al reducir la fosforilación del fosfolambano del ventrículo izquierdo en ratones LDLr-/-.O stanozolol é um esteroide que promove deposição lipídica nas artérias de camundongos LDLr-/-, entretanto, o mecanismo pelo qual a dislipidemia promove disfunção cardíaca nesses animais, ainda é pouco entendida. Deste modo, o objetivo do presente estudo é avaliar o efeito do stanozolol na contratilidade cardíaca e a participação da fosforilação da proteína fosfolambam (pPBL) miocárdica no modelo animal de aterosclerose. Os camundongos knock-out para receptor de LDL (LDLr-/-) foram alimentados com dieta padrão para biotérios e receberam semanalmente injeções subcutâneas com salina (grupo controle, C) ou 20 mg/kg de stanozolol (grupo S). Depois de oito semanas de tratamento, os parâmetros hemodinâmicos foram avaliados no ventrículo esquerdo. O coração foi então coletado, pesado para determinação da hipertrofia e armazenado em tampão formalina para a determinação das análises morfométrica (H&E) e da quantificação de colágeno (picrossirius). A expressão da proteína fosfolambam (PBL) e da sua forma fosforilada (p-PBL) no ventrículo esquerdo foi determinado por western blot. Nós observamos que o tratamento com stanozolol favoreceu a hipertrofia e a deposição de colágeno no tecido cardíaco. Além disso, o stanozolol induziu a disfunção do ventrículo esquerdo, aumento da expressão do PBL e a redução da razão p-PBL/PBL. Em conjunto, nossos dados mostram que o stanozolol promove remodelamento cardíaco e disfunção ventricular pela redução da fosforilação do fosfolambam no ventrículo esquerdo em camundongos LDLr-/-.Research, Society and Development2022-03-31info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://rsdjournal.org/index.php/rsd/article/view/2787610.33448/rsd-v11i5.27876Research, Society and Development; Vol. 11 No. 5; e12911527876Research, Society and Development; Vol. 11 Núm. 5; e12911527876Research, Society and Development; v. 11 n. 5; e129115278762525-3409reponame:Research, Society and Developmentinstname:Universidade Federal de Itajubá (UNIFEI)instacron:UNIFEIenghttps://rsdjournal.org/index.php/rsd/article/view/27876/24396Copyright (c) 2022 Tadeu Uggere de Andrade; Dionisio Dubois Fillho; Cristiane Lyrio da Silva; Mirian de Almeida Silva; Simone Alves de Almeida; Andrews Marques do Nascimento; Nazaré Souza Bissoli; Girlandia Alexandre Brasil; Ewelyne Miranda de Limahttps://creativecommons.org/licenses/by/4.0info:eu-repo/semantics/openAccessAndrade, Tadeu Uggere de Dubois Fillho, DionisioSilva, Cristiane Lyrio da Silva, Mirian de Almeida Almeida, Simone Alves de Nascimento, Andrews Marques do Bissoli, Nazaré Souza Brasil, Girlandia AlexandreLima, Ewelyne Miranda de 2022-04-17T18:18:56Zoai:ojs.pkp.sfu.ca:article/27876Revistahttps://rsdjournal.org/index.php/rsd/indexPUBhttps://rsdjournal.org/index.php/rsd/oairsd.articles@gmail.com2525-34092525-3409opendoar:2024-01-17T09:45:28.063267Research, Society and Development - Universidade Federal de Itajubá (UNIFEI)false
dc.title.none.fl_str_mv Stanozolol induces ventricular dysfunction by decreasing phospholamban phosphorylation in heart tissue of LDLr-/- mice
El estanozolol induce disfunción ventricular al reducir la fosforilación de fosfolamban en el tejido cardíaco de ratones LDLr-/-
O estanozolol induz disfunção ventricular pela redução da fosforilação do fosfolambam no tecido cardíaco de camundongos LDLr-/-
title Stanozolol induces ventricular dysfunction by decreasing phospholamban phosphorylation in heart tissue of LDLr-/- mice
spellingShingle Stanozolol induces ventricular dysfunction by decreasing phospholamban phosphorylation in heart tissue of LDLr-/- mice
Andrade, Tadeu Uggere de
Anabolic androgenic steroids
Hemodynamic parameters
Cardiac remodeling
Phospholamban phosphorylation.
Esteróide anabolico androgênico
Parâmetros hemodinâmicos
Remodelamento cardíaco
Fosfolambam fosforilada.
Esteroide androgénico anabólico
Parámetros hemodinâmicos
Remodelado cardíaco
Fosfolambano fosforilado.
title_short Stanozolol induces ventricular dysfunction by decreasing phospholamban phosphorylation in heart tissue of LDLr-/- mice
title_full Stanozolol induces ventricular dysfunction by decreasing phospholamban phosphorylation in heart tissue of LDLr-/- mice
title_fullStr Stanozolol induces ventricular dysfunction by decreasing phospholamban phosphorylation in heart tissue of LDLr-/- mice
title_full_unstemmed Stanozolol induces ventricular dysfunction by decreasing phospholamban phosphorylation in heart tissue of LDLr-/- mice
title_sort Stanozolol induces ventricular dysfunction by decreasing phospholamban phosphorylation in heart tissue of LDLr-/- mice
author Andrade, Tadeu Uggere de
author_facet Andrade, Tadeu Uggere de
Dubois Fillho, Dionisio
Silva, Cristiane Lyrio da
Silva, Mirian de Almeida
Almeida, Simone Alves de
Nascimento, Andrews Marques do
Bissoli, Nazaré Souza
Brasil, Girlandia Alexandre
Lima, Ewelyne Miranda de
author_role author
author2 Dubois Fillho, Dionisio
Silva, Cristiane Lyrio da
Silva, Mirian de Almeida
Almeida, Simone Alves de
Nascimento, Andrews Marques do
Bissoli, Nazaré Souza
Brasil, Girlandia Alexandre
Lima, Ewelyne Miranda de
author2_role author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Andrade, Tadeu Uggere de
Dubois Fillho, Dionisio
Silva, Cristiane Lyrio da
Silva, Mirian de Almeida
Almeida, Simone Alves de
Nascimento, Andrews Marques do
Bissoli, Nazaré Souza
Brasil, Girlandia Alexandre
Lima, Ewelyne Miranda de
dc.subject.por.fl_str_mv Anabolic androgenic steroids
Hemodynamic parameters
Cardiac remodeling
Phospholamban phosphorylation.
Esteróide anabolico androgênico
Parâmetros hemodinâmicos
Remodelamento cardíaco
Fosfolambam fosforilada.
Esteroide androgénico anabólico
Parámetros hemodinâmicos
Remodelado cardíaco
Fosfolambano fosforilado.
topic Anabolic androgenic steroids
Hemodynamic parameters
Cardiac remodeling
Phospholamban phosphorylation.
Esteróide anabolico androgênico
Parâmetros hemodinâmicos
Remodelamento cardíaco
Fosfolambam fosforilada.
Esteroide androgénico anabólico
Parámetros hemodinâmicos
Remodelado cardíaco
Fosfolambano fosforilado.
description Stanozolol is a steroid that causes lipid deposition in LDLr-/- mice, although the mechanism by which this dyslipidemia results in cardiac dysfunction is little understood. The aim of this study was to evaluate the effect of stanozolol on cardiac contractility and the participation of myocardial phospholamban (pPLB) phosphorylation in an atherosclerosis mouse model. LDL receptor knockout mice (LDLr-/-) were fed a standard chow diet and received weekly subcutaneous injections of either saline (control, C group) or 20 mg/kg stanozolol (S group). After 8 weeks, hemodynamic parameters were assessed in the left ventricle. The heart was collected, weighted for hypertrophy evaluation, and kept in formalin buffer for morphometric analysis (H&E) and collagen quantification (Picrossirius). Protein expression of PLB and its phosphorylated form (p-PLB) in the left ventricle was determined by western blot. We observed that stanozolol treatment favored cardiac hypertrophy and collagen deposition in heart tissue. Also, stanozolol induced left ventricle dysfunction, increasing PBL expression and decreasing the p-PLB/PLB ratio. Altogether, our data showed that stanozolol causes cardiac remodeling and ventricular dysfunction by decreasing PLB phosphorylation in the left ventricle of LDLr-/- mice.
publishDate 2022
dc.date.none.fl_str_mv 2022-03-31
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://rsdjournal.org/index.php/rsd/article/view/27876
10.33448/rsd-v11i5.27876
url https://rsdjournal.org/index.php/rsd/article/view/27876
identifier_str_mv 10.33448/rsd-v11i5.27876
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://rsdjournal.org/index.php/rsd/article/view/27876/24396
dc.rights.driver.fl_str_mv https://creativecommons.org/licenses/by/4.0
info:eu-repo/semantics/openAccess
rights_invalid_str_mv 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 Research, Society and Development
publisher.none.fl_str_mv Research, Society and Development
dc.source.none.fl_str_mv Research, Society and Development; Vol. 11 No. 5; e12911527876
Research, Society and Development; Vol. 11 Núm. 5; e12911527876
Research, Society and Development; v. 11 n. 5; e12911527876
2525-3409
reponame:Research, Society and Development
instname:Universidade Federal de Itajubá (UNIFEI)
instacron:UNIFEI
instname_str Universidade Federal de Itajubá (UNIFEI)
instacron_str UNIFEI
institution UNIFEI
reponame_str Research, Society and Development
collection Research, Society and Development
repository.name.fl_str_mv Research, Society and Development - Universidade Federal de Itajubá (UNIFEI)
repository.mail.fl_str_mv rsd.articles@gmail.com
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