Myocardial myostatin in spontaneously hypertensive rats with heart failure

Detalhes bibliográficos
Autor(a) principal: Damatto, R. L. [UNESP]
Data de Publicação: 2016
Outros Autores: Lima, A. R.R. [UNESP], Martinez, P. F., Cezar, M. D.M. [UNESP], Okoshi, K. [UNESP], Okoshi, M. P. [UNESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.1016/j.ijcard.2016.04.101
http://hdl.handle.net/11449/172864
Resumo: Background Myostatin has been shown to regulate skeletal and cardiac muscle growth. However, its status on long-term hypertrophied myocardium has not been addressed. The purpose of this study was to evaluate the expression of myocardial myostatin and its antagonist follistatin in spontaneously hypertensive rats (SHR) with heart failure. Methods Eighteen-month-old SHR were evaluated to identify clinical features of heart failure such as tachypnea/labored respiration and weight loss. After heart failure was detected, rats were subjected to echocardiogram and euthanized. Age-matched normotensive Wistar-Kyoto (WKY) rats were used as controls. Myostatin and follistatin protein expression was assessed by Western blotting. Statistical analysis was performed by Student's t test. Results All SHR (n = 8) presented right ventricular hypertrophy and five had lung congestion. SHR had left chambers hypertrophy and dilation (left atrial diameter: WKY 5.73 ± 0.59; SHR 7.28 ± 1.17 mm; p = 0.004; left ventricular (LV) diastolic diameter/body weight ratio: WKY 19.6 ± 3.1; SHR 27.7 ± 4.7 mm/kg; p = 0.001), and LV systolic dysfunction (midwall fractional shortening: WKY 34.9 ± 3.31; SHR 24.8 ± 3.20%; p = 0.003). Myocyte diameter (WKY 23.1 ± 1.50, SHR 25.5 ± 1.33 μm; p = 0.004) and myocardial interstitial collagen fraction (WKY 4.86 ± 0.01; SHR 8.36 ± 0.02%; p < 0.001) were increased in the SHR. Myostatin (WKY 1.00 ± 0.16; SHR 0.77 ± 0.23 arbitrary units; p = 0.035) and follistatin (WKY 1.00 ± 0.35; SHR 0.49 ± 0.18 arbitrary units; p = 0.002) expression was lower in SHR. Myostatin and follistatin expression negatively correlated with LV diastolic diameter-to-body weight ratio and LV systolic diameter, and positively correlated with midwall fractional shortening. Conclusion Myostatin and follistatin protein expression is reduced in the long-term hypertrophied myocardium from spontaneously hypertensive rats with heart failure.
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spelling Myocardial myostatin in spontaneously hypertensive rats with heart failureCardiac failureCardiac remodelingFollistatinMyocardiumMyostatinSpontaneously hypertensive ratBackground Myostatin has been shown to regulate skeletal and cardiac muscle growth. However, its status on long-term hypertrophied myocardium has not been addressed. The purpose of this study was to evaluate the expression of myocardial myostatin and its antagonist follistatin in spontaneously hypertensive rats (SHR) with heart failure. Methods Eighteen-month-old SHR were evaluated to identify clinical features of heart failure such as tachypnea/labored respiration and weight loss. After heart failure was detected, rats were subjected to echocardiogram and euthanized. Age-matched normotensive Wistar-Kyoto (WKY) rats were used as controls. Myostatin and follistatin protein expression was assessed by Western blotting. Statistical analysis was performed by Student's t test. Results All SHR (n = 8) presented right ventricular hypertrophy and five had lung congestion. SHR had left chambers hypertrophy and dilation (left atrial diameter: WKY 5.73 ± 0.59; SHR 7.28 ± 1.17 mm; p = 0.004; left ventricular (LV) diastolic diameter/body weight ratio: WKY 19.6 ± 3.1; SHR 27.7 ± 4.7 mm/kg; p = 0.001), and LV systolic dysfunction (midwall fractional shortening: WKY 34.9 ± 3.31; SHR 24.8 ± 3.20%; p = 0.003). Myocyte diameter (WKY 23.1 ± 1.50, SHR 25.5 ± 1.33 μm; p = 0.004) and myocardial interstitial collagen fraction (WKY 4.86 ± 0.01; SHR 8.36 ± 0.02%; p < 0.001) were increased in the SHR. Myostatin (WKY 1.00 ± 0.16; SHR 0.77 ± 0.23 arbitrary units; p = 0.035) and follistatin (WKY 1.00 ± 0.35; SHR 0.49 ± 0.18 arbitrary units; p = 0.002) expression was lower in SHR. Myostatin and follistatin expression negatively correlated with LV diastolic diameter-to-body weight ratio and LV systolic diameter, and positively correlated with midwall fractional shortening. Conclusion Myostatin and follistatin protein expression is reduced in the long-term hypertrophied myocardium from spontaneously hypertensive rats with heart failure.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Department of Internal Medicine Botucatu Medical School Sao Paulo State University UNESPFederal University of Mato Grosso Do sul UFMSDepartamento de Clinica Medica Faculdade de Medicina de Botucatu UNESP, Rubiao Junior, S/NDepartment of Internal Medicine Botucatu Medical School Sao Paulo State University UNESPDepartamento de Clinica Medica Faculdade de Medicina de Botucatu UNESP, Rubiao Junior, S/NFAPESP: 2009/54857-4FAPESP: 2012/50512-5CNPq: 306770/2015-6CNPq: 308674/2015-4Universidade Estadual Paulista (Unesp)Universidade Federal de Mato Grosso do Sul (UFMS)Damatto, R. L. [UNESP]Lima, A. R.R. [UNESP]Martinez, P. F.Cezar, M. D.M. [UNESP]Okoshi, K. [UNESP]Okoshi, M. P. [UNESP]2018-12-11T17:02:29Z2018-12-11T17:02:29Z2016-07-15info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article384-387application/pdfhttp://dx.doi.org/10.1016/j.ijcard.2016.04.101International Journal of Cardiology, v. 215, p. 384-387.1874-17540167-5273http://hdl.handle.net/11449/17286410.1016/j.ijcard.2016.04.1012-s2.0-849642647372-s2.0-84964264737.pdfScopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengInternational Journal of Cardiology1,200info:eu-repo/semantics/openAccess2024-08-14T17:22:13Zoai:repositorio.unesp.br:11449/172864Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-14T17:22:13Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Myocardial myostatin in spontaneously hypertensive rats with heart failure
title Myocardial myostatin in spontaneously hypertensive rats with heart failure
spellingShingle Myocardial myostatin in spontaneously hypertensive rats with heart failure
Damatto, R. L. [UNESP]
Cardiac failure
Cardiac remodeling
Follistatin
Myocardium
Myostatin
Spontaneously hypertensive rat
title_short Myocardial myostatin in spontaneously hypertensive rats with heart failure
title_full Myocardial myostatin in spontaneously hypertensive rats with heart failure
title_fullStr Myocardial myostatin in spontaneously hypertensive rats with heart failure
title_full_unstemmed Myocardial myostatin in spontaneously hypertensive rats with heart failure
title_sort Myocardial myostatin in spontaneously hypertensive rats with heart failure
author Damatto, R. L. [UNESP]
author_facet Damatto, R. L. [UNESP]
Lima, A. R.R. [UNESP]
Martinez, P. F.
Cezar, M. D.M. [UNESP]
Okoshi, K. [UNESP]
Okoshi, M. P. [UNESP]
author_role author
author2 Lima, A. R.R. [UNESP]
Martinez, P. F.
Cezar, M. D.M. [UNESP]
Okoshi, K. [UNESP]
Okoshi, M. P. [UNESP]
author2_role author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade Estadual Paulista (Unesp)
Universidade Federal de Mato Grosso do Sul (UFMS)
dc.contributor.author.fl_str_mv Damatto, R. L. [UNESP]
Lima, A. R.R. [UNESP]
Martinez, P. F.
Cezar, M. D.M. [UNESP]
Okoshi, K. [UNESP]
Okoshi, M. P. [UNESP]
dc.subject.por.fl_str_mv Cardiac failure
Cardiac remodeling
Follistatin
Myocardium
Myostatin
Spontaneously hypertensive rat
topic Cardiac failure
Cardiac remodeling
Follistatin
Myocardium
Myostatin
Spontaneously hypertensive rat
description Background Myostatin has been shown to regulate skeletal and cardiac muscle growth. However, its status on long-term hypertrophied myocardium has not been addressed. The purpose of this study was to evaluate the expression of myocardial myostatin and its antagonist follistatin in spontaneously hypertensive rats (SHR) with heart failure. Methods Eighteen-month-old SHR were evaluated to identify clinical features of heart failure such as tachypnea/labored respiration and weight loss. After heart failure was detected, rats were subjected to echocardiogram and euthanized. Age-matched normotensive Wistar-Kyoto (WKY) rats were used as controls. Myostatin and follistatin protein expression was assessed by Western blotting. Statistical analysis was performed by Student's t test. Results All SHR (n = 8) presented right ventricular hypertrophy and five had lung congestion. SHR had left chambers hypertrophy and dilation (left atrial diameter: WKY 5.73 ± 0.59; SHR 7.28 ± 1.17 mm; p = 0.004; left ventricular (LV) diastolic diameter/body weight ratio: WKY 19.6 ± 3.1; SHR 27.7 ± 4.7 mm/kg; p = 0.001), and LV systolic dysfunction (midwall fractional shortening: WKY 34.9 ± 3.31; SHR 24.8 ± 3.20%; p = 0.003). Myocyte diameter (WKY 23.1 ± 1.50, SHR 25.5 ± 1.33 μm; p = 0.004) and myocardial interstitial collagen fraction (WKY 4.86 ± 0.01; SHR 8.36 ± 0.02%; p < 0.001) were increased in the SHR. Myostatin (WKY 1.00 ± 0.16; SHR 0.77 ± 0.23 arbitrary units; p = 0.035) and follistatin (WKY 1.00 ± 0.35; SHR 0.49 ± 0.18 arbitrary units; p = 0.002) expression was lower in SHR. Myostatin and follistatin expression negatively correlated with LV diastolic diameter-to-body weight ratio and LV systolic diameter, and positively correlated with midwall fractional shortening. Conclusion Myostatin and follistatin protein expression is reduced in the long-term hypertrophied myocardium from spontaneously hypertensive rats with heart failure.
publishDate 2016
dc.date.none.fl_str_mv 2016-07-15
2018-12-11T17:02:29Z
2018-12-11T17:02:29Z
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.ijcard.2016.04.101
International Journal of Cardiology, v. 215, p. 384-387.
1874-1754
0167-5273
http://hdl.handle.net/11449/172864
10.1016/j.ijcard.2016.04.101
2-s2.0-84964264737
2-s2.0-84964264737.pdf
url http://dx.doi.org/10.1016/j.ijcard.2016.04.101
http://hdl.handle.net/11449/172864
identifier_str_mv International Journal of Cardiology, v. 215, p. 384-387.
1874-1754
0167-5273
10.1016/j.ijcard.2016.04.101
2-s2.0-84964264737
2-s2.0-84964264737.pdf
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv International Journal of Cardiology
1,200
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 384-387
application/pdf
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
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