Heart failure-induced skeletal myopathy in spontaneously hypertensive rats

Detalhes bibliográficos
Autor(a) principal: Damatto, R. L. [UNESP]
Data de Publicação: 2013
Outros Autores: Martinez, P. F. [UNESP], Lima, A. R R [UNESP], Cezar, M. D M [UNESP], Campos, D. H S [UNESP], Oliveira Junior, S. A. [UNESP], Guizoni, D. M. [UNESP], Bonomo, C. [UNESP], Nakatani, B. T. [UNESP], Dal Pai Silva, M. [UNESP], Carvalho, R. F. [UNESP], Okoshi, Katashi [UNESP], Okoshi, Marina Politi [UNESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.1016/j.ijcard.2012.03.063
http://hdl.handle.net/11449/76249
Resumo: Background: Although skeletal muscle atrophy and changes in myosin heavy chain (MyHC) isoforms have often been observed during heart failure, their pathophysiological mechanisms are not completely defined. In this study we tested the hypothesis that skeletal muscle phenotype changes are related to myogenic regulatory factors and myostatin/follistatin expression in spontaneously hypertensive rats (SHR) with heart failure. Methods: After developing tachypnea, SHR were subjected to transthoracic echocardiogram. Pathological evidence of heart failure was assessed during euthanasia. Age-matched Wistar-Kyoto (WKY) rats were used as controls. Soleus muscle morphometry was analyzed in histological sections, and MyHC isoforms evaluated by electrophoresis. Protein levels were assessed by Western blotting. Statistical analysis: Student's t test and Pearson correlation. Results: All SHR presented right ventricular hypertrophy and seven had pleuropericardial effusion. Echocardiographic evaluation showed dilation in the left chambers and left ventricular hypertrophy with systolic and diastolic dysfunction in SHR. Soleus weight and fiber cross sectional areas were lower (WKY 3615±412; SHR 2035±224 μm2; P < 0.001), and collagen fractional volume was higher in SHR. The relative amount of type I MyHC isoform was increased in SHR. Myogenin, myostatin, and follistatin expression was lower and MRF4 levels higher in SHR. Myogenin and follistatin expression positively correlated with fiber cross sectional areas and MRF4 levels positively correlated with I MyHC isoform. Conclusion: Reduced myogenin and follistatin expression seems to participate in muscle atrophy while increased MRF4 protein levels can modulate myosin heavy chain isoform shift in skeletal muscle of spontaneously hypertensive rats with heart failure. © 2012 Elsevier B.V.
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spelling Heart failure-induced skeletal myopathy in spontaneously hypertensive ratsFibrosisHeart failureMuscle atrophyMyosin heavy chainSkeletal myopathySpontaneously hypertensive ratfollistatinmyogenic factormyogeninmyosin heavy chainmyostatinanimal experimentanimal modelaortacontrolled studyheart failureheart left atriumheart left ventricle ejection fractionheart left ventricle hypertrophyheart rateheart right ventricle hypertrophyheart sizemalemuscle atrophymyofibrosismyopathynonhumanpericardial effusionphenotypepriority journalprotein expressionratskeletal musclesoleus musclespontaneously hypertensive ratBackground: Although skeletal muscle atrophy and changes in myosin heavy chain (MyHC) isoforms have often been observed during heart failure, their pathophysiological mechanisms are not completely defined. In this study we tested the hypothesis that skeletal muscle phenotype changes are related to myogenic regulatory factors and myostatin/follistatin expression in spontaneously hypertensive rats (SHR) with heart failure. Methods: After developing tachypnea, SHR were subjected to transthoracic echocardiogram. Pathological evidence of heart failure was assessed during euthanasia. Age-matched Wistar-Kyoto (WKY) rats were used as controls. Soleus muscle morphometry was analyzed in histological sections, and MyHC isoforms evaluated by electrophoresis. Protein levels were assessed by Western blotting. Statistical analysis: Student's t test and Pearson correlation. Results: All SHR presented right ventricular hypertrophy and seven had pleuropericardial effusion. Echocardiographic evaluation showed dilation in the left chambers and left ventricular hypertrophy with systolic and diastolic dysfunction in SHR. Soleus weight and fiber cross sectional areas were lower (WKY 3615±412; SHR 2035±224 μm2; P < 0.001), and collagen fractional volume was higher in SHR. The relative amount of type I MyHC isoform was increased in SHR. Myogenin, myostatin, and follistatin expression was lower and MRF4 levels higher in SHR. Myogenin and follistatin expression positively correlated with fiber cross sectional areas and MRF4 levels positively correlated with I MyHC isoform. Conclusion: Reduced myogenin and follistatin expression seems to participate in muscle atrophy while increased MRF4 protein levels can modulate myosin heavy chain isoform shift in skeletal muscle of spontaneously hypertensive rats with heart failure. © 2012 Elsevier B.V.Department of Internal Medicine Botucatu Medical School Sao Paulo State UniversityDepartamento de Clinica Medica Faculdade de Medicina de Botucatu UNESP, Rubiao Junior, S/N 18618-970, Botucatu, SPFederal University of Mato Grosso Do sul Campo GrandeDepartment of Morphology Institute of Biosciences Sao Paulo State UniversityDepartamento de Morfologia Instituto de Biociencias, Rubiao Junior S/N, Botucatu, SPDepartment of Internal Medicine Botucatu Medical School Sao Paulo State UniversityDepartamento de Clinica Medica Faculdade de Medicina de Botucatu UNESP, Rubiao Junior, S/N 18618-970, Botucatu, SPDepartment of Morphology Institute of Biosciences Sao Paulo State UniversityUniversidade Estadual Paulista (Unesp)Campo GrandeInstituto de BiocienciasDamatto, R. L. [UNESP]Martinez, P. F. [UNESP]Lima, A. R R [UNESP]Cezar, M. D M [UNESP]Campos, D. H S [UNESP]Oliveira Junior, S. A. [UNESP]Guizoni, D. M. [UNESP]Bonomo, C. [UNESP]Nakatani, B. T. [UNESP]Dal Pai Silva, M. [UNESP]Carvalho, R. F. [UNESP]Okoshi, Katashi [UNESP]Okoshi, Marina Politi [UNESP]2014-05-27T11:30:08Z2014-05-27T11:30:08Z2013-08-10info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article698-703application/pdfhttp://dx.doi.org/10.1016/j.ijcard.2012.03.063International Journal of Cardiology, v. 167, n. 3, p. 698-703, 2013.0167-52731874-1754http://hdl.handle.net/11449/7624910.1016/j.ijcard.2012.03.063WOS:0003223195000232-s2.0-848809218242-s2.0-84880921824.pdf1590971576309420446313867199843241253447531004540000-0003-1270-7372Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengInternational Journal of Cardiology4.0341,200info:eu-repo/semantics/openAccess2024-08-14T17:23:09Zoai:repositorio.unesp.br:11449/76249Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-14T17:23:09Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Heart failure-induced skeletal myopathy in spontaneously hypertensive rats
title Heart failure-induced skeletal myopathy in spontaneously hypertensive rats
spellingShingle Heart failure-induced skeletal myopathy in spontaneously hypertensive rats
Damatto, R. L. [UNESP]
Fibrosis
Heart failure
Muscle atrophy
Myosin heavy chain
Skeletal myopathy
Spontaneously hypertensive rat
follistatin
myogenic factor
myogenin
myosin heavy chain
myostatin
animal experiment
animal model
aorta
controlled study
heart failure
heart left atrium
heart left ventricle ejection fraction
heart left ventricle hypertrophy
heart rate
heart right ventricle hypertrophy
heart size
male
muscle atrophy
myofibrosis
myopathy
nonhuman
pericardial effusion
phenotype
priority journal
protein expression
rat
skeletal muscle
soleus muscle
spontaneously hypertensive rat
title_short Heart failure-induced skeletal myopathy in spontaneously hypertensive rats
title_full Heart failure-induced skeletal myopathy in spontaneously hypertensive rats
title_fullStr Heart failure-induced skeletal myopathy in spontaneously hypertensive rats
title_full_unstemmed Heart failure-induced skeletal myopathy in spontaneously hypertensive rats
title_sort Heart failure-induced skeletal myopathy in spontaneously hypertensive rats
author Damatto, R. L. [UNESP]
author_facet Damatto, R. L. [UNESP]
Martinez, P. F. [UNESP]
Lima, A. R R [UNESP]
Cezar, M. D M [UNESP]
Campos, D. H S [UNESP]
Oliveira Junior, S. A. [UNESP]
Guizoni, D. M. [UNESP]
Bonomo, C. [UNESP]
Nakatani, B. T. [UNESP]
Dal Pai Silva, M. [UNESP]
Carvalho, R. F. [UNESP]
Okoshi, Katashi [UNESP]
Okoshi, Marina Politi [UNESP]
author_role author
author2 Martinez, P. F. [UNESP]
Lima, A. R R [UNESP]
Cezar, M. D M [UNESP]
Campos, D. H S [UNESP]
Oliveira Junior, S. A. [UNESP]
Guizoni, D. M. [UNESP]
Bonomo, C. [UNESP]
Nakatani, B. T. [UNESP]
Dal Pai Silva, M. [UNESP]
Carvalho, R. F. [UNESP]
Okoshi, Katashi [UNESP]
Okoshi, Marina Politi [UNESP]
author2_role author
author
author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade Estadual Paulista (Unesp)
Campo Grande
Instituto de Biociencias
dc.contributor.author.fl_str_mv Damatto, R. L. [UNESP]
Martinez, P. F. [UNESP]
Lima, A. R R [UNESP]
Cezar, M. D M [UNESP]
Campos, D. H S [UNESP]
Oliveira Junior, S. A. [UNESP]
Guizoni, D. M. [UNESP]
Bonomo, C. [UNESP]
Nakatani, B. T. [UNESP]
Dal Pai Silva, M. [UNESP]
Carvalho, R. F. [UNESP]
Okoshi, Katashi [UNESP]
Okoshi, Marina Politi [UNESP]
dc.subject.por.fl_str_mv Fibrosis
Heart failure
Muscle atrophy
Myosin heavy chain
Skeletal myopathy
Spontaneously hypertensive rat
follistatin
myogenic factor
myogenin
myosin heavy chain
myostatin
animal experiment
animal model
aorta
controlled study
heart failure
heart left atrium
heart left ventricle ejection fraction
heart left ventricle hypertrophy
heart rate
heart right ventricle hypertrophy
heart size
male
muscle atrophy
myofibrosis
myopathy
nonhuman
pericardial effusion
phenotype
priority journal
protein expression
rat
skeletal muscle
soleus muscle
spontaneously hypertensive rat
topic Fibrosis
Heart failure
Muscle atrophy
Myosin heavy chain
Skeletal myopathy
Spontaneously hypertensive rat
follistatin
myogenic factor
myogenin
myosin heavy chain
myostatin
animal experiment
animal model
aorta
controlled study
heart failure
heart left atrium
heart left ventricle ejection fraction
heart left ventricle hypertrophy
heart rate
heart right ventricle hypertrophy
heart size
male
muscle atrophy
myofibrosis
myopathy
nonhuman
pericardial effusion
phenotype
priority journal
protein expression
rat
skeletal muscle
soleus muscle
spontaneously hypertensive rat
description Background: Although skeletal muscle atrophy and changes in myosin heavy chain (MyHC) isoforms have often been observed during heart failure, their pathophysiological mechanisms are not completely defined. In this study we tested the hypothesis that skeletal muscle phenotype changes are related to myogenic regulatory factors and myostatin/follistatin expression in spontaneously hypertensive rats (SHR) with heart failure. Methods: After developing tachypnea, SHR were subjected to transthoracic echocardiogram. Pathological evidence of heart failure was assessed during euthanasia. Age-matched Wistar-Kyoto (WKY) rats were used as controls. Soleus muscle morphometry was analyzed in histological sections, and MyHC isoforms evaluated by electrophoresis. Protein levels were assessed by Western blotting. Statistical analysis: Student's t test and Pearson correlation. Results: All SHR presented right ventricular hypertrophy and seven had pleuropericardial effusion. Echocardiographic evaluation showed dilation in the left chambers and left ventricular hypertrophy with systolic and diastolic dysfunction in SHR. Soleus weight and fiber cross sectional areas were lower (WKY 3615±412; SHR 2035±224 μm2; P < 0.001), and collagen fractional volume was higher in SHR. The relative amount of type I MyHC isoform was increased in SHR. Myogenin, myostatin, and follistatin expression was lower and MRF4 levels higher in SHR. Myogenin and follistatin expression positively correlated with fiber cross sectional areas and MRF4 levels positively correlated with I MyHC isoform. Conclusion: Reduced myogenin and follistatin expression seems to participate in muscle atrophy while increased MRF4 protein levels can modulate myosin heavy chain isoform shift in skeletal muscle of spontaneously hypertensive rats with heart failure. © 2012 Elsevier B.V.
publishDate 2013
dc.date.none.fl_str_mv 2013-08-10
2014-05-27T11:30:08Z
2014-05-27T11:30:08Z
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.2012.03.063
International Journal of Cardiology, v. 167, n. 3, p. 698-703, 2013.
0167-5273
1874-1754
http://hdl.handle.net/11449/76249
10.1016/j.ijcard.2012.03.063
WOS:000322319500023
2-s2.0-84880921824
2-s2.0-84880921824.pdf
1590971576309420
4463138671998432
4125344753100454
0000-0003-1270-7372
url http://dx.doi.org/10.1016/j.ijcard.2012.03.063
http://hdl.handle.net/11449/76249
identifier_str_mv International Journal of Cardiology, v. 167, n. 3, p. 698-703, 2013.
0167-5273
1874-1754
10.1016/j.ijcard.2012.03.063
WOS:000322319500023
2-s2.0-84880921824
2-s2.0-84880921824.pdf
1590971576309420
4463138671998432
4125344753100454
0000-0003-1270-7372
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv International Journal of Cardiology
4.034
1,200
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 698-703
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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