Stanozolol induces ventricular dysfunction by decreasing phospholamban phosphorylation in heart tissue of LDLr-/- mice
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , , , , , , , |
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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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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1797052708435263488 |