Heart Failure-Induced Diaphragm Myopathy
Autor(a) principal: | |
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Data de Publicação: | 2014 |
Outros Autores: | , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1159/000363003 http://hdl.handle.net/11449/117256 |
Resumo: | Background: Intracellular signaling pathways involved in skeletal myosin heavy chain (MyHC) isofornn alterations during heart failure (HF) are not completely understood. We tested the hypothesis that diaphragm expression of mitogen-activated protein kinases (MAPK) and myogenic regulatory factors is changed in rats with myocardial infarction (MI) induced HF. Methods: Six months after MI rats were subjected to transthoracic echocardiography. After euthanasia, infarcted rats were subdivided in MI/HF- group (with no HF evidence; n=10), and MI/HF+ (with right ventricular hypertrophy and lung congestion; n=10). Sham operated rats were used as controls (n=10). MyHC isofornns were analyzed by electrophoresis. Statistical analysis: ANOVA and Pearson correlation. Results: MI/HF- had left cardiac chambers dilation with systolic and diastolic left ventricular dysfunction. Cardiac injury was more intense in MI/HF+ than MI/HF-. MyHC I isoform percentage was higher in MI/HF+ than MI/HF-, and IIb isoform lower in MI/HF+ than Sham. Left atrial diameter-to-body weight ratio positively correlated with MyHC I (p=0.005) and negatively correlated with MyHC IIb (p=0.02). TNF-alpha serum concentration positively correlated with MyHC I isoform. Total and phosphorylated ERK was lower in MI/HF- and MI/HF+ than Sham. Phosphorylated JNK was lower in MI/HF- than Sham. JNK and p38 did not differ between groups. Expression of NF-kappa B and the myogenic regulatory factors MyoD, myogenin, and MRF4 was similar between groups. Conclusion: Diaphragm MyHC fast-to-slow shift is related to cardiac dysfunction severity and TNF-alpha serum levels in infarcted rats. Reduced ERK expression seems to participate in MyHC isofornn changes. Myogenic regulatory factors and NF-kappa B do not modulate diaphragm MyHC distribution during chronic HF. Copyright (C) 2014 S. Karger AG, Basel |
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Heart Failure-Induced Diaphragm MyopathySkeletal muscleMAPKMyogenic regulatory factorsMyosin heavy chain isoformsEchocardiographyMyocardial infarctionBackground: Intracellular signaling pathways involved in skeletal myosin heavy chain (MyHC) isofornn alterations during heart failure (HF) are not completely understood. We tested the hypothesis that diaphragm expression of mitogen-activated protein kinases (MAPK) and myogenic regulatory factors is changed in rats with myocardial infarction (MI) induced HF. Methods: Six months after MI rats were subjected to transthoracic echocardiography. After euthanasia, infarcted rats were subdivided in MI/HF- group (with no HF evidence; n=10), and MI/HF+ (with right ventricular hypertrophy and lung congestion; n=10). Sham operated rats were used as controls (n=10). MyHC isofornns were analyzed by electrophoresis. Statistical analysis: ANOVA and Pearson correlation. Results: MI/HF- had left cardiac chambers dilation with systolic and diastolic left ventricular dysfunction. Cardiac injury was more intense in MI/HF+ than MI/HF-. MyHC I isoform percentage was higher in MI/HF+ than MI/HF-, and IIb isoform lower in MI/HF+ than Sham. Left atrial diameter-to-body weight ratio positively correlated with MyHC I (p=0.005) and negatively correlated with MyHC IIb (p=0.02). TNF-alpha serum concentration positively correlated with MyHC I isoform. Total and phosphorylated ERK was lower in MI/HF- and MI/HF+ than Sham. Phosphorylated JNK was lower in MI/HF- than Sham. JNK and p38 did not differ between groups. Expression of NF-kappa B and the myogenic regulatory factors MyoD, myogenin, and MRF4 was similar between groups. Conclusion: Diaphragm MyHC fast-to-slow shift is related to cardiac dysfunction severity and TNF-alpha serum levels in infarcted rats. Reduced ERK expression seems to participate in MyHC isofornn changes. Myogenic regulatory factors and NF-kappa B do not modulate diaphragm MyHC distribution during chronic HF. Copyright (C) 2014 S. Karger AG, BaselConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)UNESP, Botucatu Med Sch, Dept Internal Med, Botocutu, SP, BrazilFed Univ Mato Grosso Do Sul UFMS, Biol Sci & Hlth Ctr, Campo Grande, MS, BrazilUNESP, Biosci Inst, Dept Morphol, Botucatu, SP, BrazilUNESP, Botucatu Med Sch, Dept Internal Med, Botocutu, SP, BrazilUNESP, Biosci Inst, Dept Morphol, Botucatu, SP, BrazilCNPq: 306857/2012-0CNPq: 306845/2012-1FAPESP: 07/57499-6FAPESP: 10/50084-8FAPESP: 08/58655-4KargerUniversidade Estadual Paulista (Unesp)Universidade Federal de Mato Grosso do Sul (UFMS)Ruiz Lima, Aline Regina [UNESP]Martinez, Paula FelippeDamatto, Ricardo Luiz [UNESP]Mariano Cezar, Marcelo Diarcadia [UNESP]Guizoni, Daniele Mendes [UNESP]Bonomo, Camila [UNESP]Oliveira, Silvio AssisSilva, Maeli Dal-Pai [UNESP]Zornoff, Leonardo Antonio Mamede [UNESP]Okoshi, Katashi [UNESP]Okoshi, Marina Politi [UNESP]2015-03-18T15:55:39Z2015-03-18T15:55:39Z2014-01-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article333-345application/pdfhttp://dx.doi.org/10.1159/000363003Cellular Physiology And Biochemistry. Basel: Karger, v. 34, n. 2, p. 333-345, 2014.1015-8987http://hdl.handle.net/11449/11725610.1159/000363003WOS:000343764600010WOS000343764600010.pdf159097157630942044631386719984325016839015394547Web of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengCellular Physiology And Biochemistry5.5001,561info:eu-repo/semantics/openAccess2024-08-14T17:36:16Zoai:repositorio.unesp.br:11449/117256Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-14T17:36:16Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Heart Failure-Induced Diaphragm Myopathy |
title |
Heart Failure-Induced Diaphragm Myopathy |
spellingShingle |
Heart Failure-Induced Diaphragm Myopathy Ruiz Lima, Aline Regina [UNESP] Skeletal muscle MAPK Myogenic regulatory factors Myosin heavy chain isoforms Echocardiography Myocardial infarction |
title_short |
Heart Failure-Induced Diaphragm Myopathy |
title_full |
Heart Failure-Induced Diaphragm Myopathy |
title_fullStr |
Heart Failure-Induced Diaphragm Myopathy |
title_full_unstemmed |
Heart Failure-Induced Diaphragm Myopathy |
title_sort |
Heart Failure-Induced Diaphragm Myopathy |
author |
Ruiz Lima, Aline Regina [UNESP] |
author_facet |
Ruiz Lima, Aline Regina [UNESP] Martinez, Paula Felippe Damatto, Ricardo Luiz [UNESP] Mariano Cezar, Marcelo Diarcadia [UNESP] Guizoni, Daniele Mendes [UNESP] Bonomo, Camila [UNESP] Oliveira, Silvio Assis Silva, Maeli Dal-Pai [UNESP] Zornoff, Leonardo Antonio Mamede [UNESP] Okoshi, Katashi [UNESP] Okoshi, Marina Politi [UNESP] |
author_role |
author |
author2 |
Martinez, Paula Felippe Damatto, Ricardo Luiz [UNESP] Mariano Cezar, Marcelo Diarcadia [UNESP] Guizoni, Daniele Mendes [UNESP] Bonomo, Camila [UNESP] Oliveira, Silvio Assis Silva, Maeli Dal-Pai [UNESP] Zornoff, Leonardo Antonio Mamede [UNESP] Okoshi, Katashi [UNESP] Okoshi, Marina Politi [UNESP] |
author2_role |
author author author author author 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 |
Ruiz Lima, Aline Regina [UNESP] Martinez, Paula Felippe Damatto, Ricardo Luiz [UNESP] Mariano Cezar, Marcelo Diarcadia [UNESP] Guizoni, Daniele Mendes [UNESP] Bonomo, Camila [UNESP] Oliveira, Silvio Assis Silva, Maeli Dal-Pai [UNESP] Zornoff, Leonardo Antonio Mamede [UNESP] Okoshi, Katashi [UNESP] Okoshi, Marina Politi [UNESP] |
dc.subject.por.fl_str_mv |
Skeletal muscle MAPK Myogenic regulatory factors Myosin heavy chain isoforms Echocardiography Myocardial infarction |
topic |
Skeletal muscle MAPK Myogenic regulatory factors Myosin heavy chain isoforms Echocardiography Myocardial infarction |
description |
Background: Intracellular signaling pathways involved in skeletal myosin heavy chain (MyHC) isofornn alterations during heart failure (HF) are not completely understood. We tested the hypothesis that diaphragm expression of mitogen-activated protein kinases (MAPK) and myogenic regulatory factors is changed in rats with myocardial infarction (MI) induced HF. Methods: Six months after MI rats were subjected to transthoracic echocardiography. After euthanasia, infarcted rats were subdivided in MI/HF- group (with no HF evidence; n=10), and MI/HF+ (with right ventricular hypertrophy and lung congestion; n=10). Sham operated rats were used as controls (n=10). MyHC isofornns were analyzed by electrophoresis. Statistical analysis: ANOVA and Pearson correlation. Results: MI/HF- had left cardiac chambers dilation with systolic and diastolic left ventricular dysfunction. Cardiac injury was more intense in MI/HF+ than MI/HF-. MyHC I isoform percentage was higher in MI/HF+ than MI/HF-, and IIb isoform lower in MI/HF+ than Sham. Left atrial diameter-to-body weight ratio positively correlated with MyHC I (p=0.005) and negatively correlated with MyHC IIb (p=0.02). TNF-alpha serum concentration positively correlated with MyHC I isoform. Total and phosphorylated ERK was lower in MI/HF- and MI/HF+ than Sham. Phosphorylated JNK was lower in MI/HF- than Sham. JNK and p38 did not differ between groups. Expression of NF-kappa B and the myogenic regulatory factors MyoD, myogenin, and MRF4 was similar between groups. Conclusion: Diaphragm MyHC fast-to-slow shift is related to cardiac dysfunction severity and TNF-alpha serum levels in infarcted rats. Reduced ERK expression seems to participate in MyHC isofornn changes. Myogenic regulatory factors and NF-kappa B do not modulate diaphragm MyHC distribution during chronic HF. Copyright (C) 2014 S. Karger AG, Basel |
publishDate |
2014 |
dc.date.none.fl_str_mv |
2014-01-01 2015-03-18T15:55:39Z 2015-03-18T15:55:39Z |
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/10.1159/000363003 Cellular Physiology And Biochemistry. Basel: Karger, v. 34, n. 2, p. 333-345, 2014. 1015-8987 http://hdl.handle.net/11449/117256 10.1159/000363003 WOS:000343764600010 WOS000343764600010.pdf 1590971576309420 4463138671998432 5016839015394547 |
url |
http://dx.doi.org/10.1159/000363003 http://hdl.handle.net/11449/117256 |
identifier_str_mv |
Cellular Physiology And Biochemistry. Basel: Karger, v. 34, n. 2, p. 333-345, 2014. 1015-8987 10.1159/000363003 WOS:000343764600010 WOS000343764600010.pdf 1590971576309420 4463138671998432 5016839015394547 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Cellular Physiology And Biochemistry 5.500 1,561 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
333-345 application/pdf |
dc.publisher.none.fl_str_mv |
Karger |
publisher.none.fl_str_mv |
Karger |
dc.source.none.fl_str_mv |
Web of Science 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_ |
1808128184869191680 |