Myocardial myostatin in spontaneously hypertensive rats with heart failure
Autor(a) principal: | |
---|---|
Data de Publicação: | 2016 |
Outros Autores: | , , , , |
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. |
id |
UNSP_219e32d100391049c72ec8324a464bd4 |
---|---|
oai_identifier_str |
oai:repositorio.unesp.br:11449/172864 |
network_acronym_str |
UNSP |
network_name_str |
Repositório Institucional da UNESP |
repository_id_str |
2946 |
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 |
|
_version_ |
1808128112606576640 |