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dc.contributor.authorDamatto, R. L.-
dc.contributor.authorMartinez, P. F.-
dc.contributor.authorLima, A. R R-
dc.contributor.authorCezar, M. D M-
dc.contributor.authorCampos, D. H S-
dc.contributor.authorOliveira Junior, S. A.-
dc.contributor.authorGuizoni, D. M.-
dc.contributor.authorBonomo, C.-
dc.contributor.authorNakatani, B. T.-
dc.contributor.authorDal Pai Silva, M.-
dc.contributor.authorCarvalho, R. F.-
dc.contributor.authorOkoshi, Katashi-
dc.contributor.authorOkoshi, Marina Politi-
dc.identifier.citationInternational Journal of Cardiology, v. 167, n. 3, p. 698-703, 2013.-
dc.description.abstractBackground: 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.en
dc.subjectHeart failure-
dc.subjectMuscle atrophy-
dc.subjectMyosin heavy chain-
dc.subjectSkeletal myopathy-
dc.subjectSpontaneously hypertensive rat-
dc.subjectmyogenic factor-
dc.subjectmyosin heavy chain-
dc.subjectanimal experiment-
dc.subjectanimal model-
dc.subjectcontrolled study-
dc.subjectheart failure-
dc.subjectheart left atrium-
dc.subjectheart left ventricle ejection fraction-
dc.subjectheart left ventricle hypertrophy-
dc.subjectheart rate-
dc.subjectheart right ventricle hypertrophy-
dc.subjectheart size-
dc.subjectmuscle atrophy-
dc.subjectpericardial effusion-
dc.subjectpriority journal-
dc.subjectprotein expression-
dc.subjectskeletal muscle-
dc.subjectsoleus muscle-
dc.subjectspontaneously hypertensive rat-
dc.titleHeart failure-induced skeletal myopathy in spontaneously hypertensive ratsen
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.contributor.institutionCampo Grande-
dc.contributor.institutionInstituto de Biociencias-
dc.description.affiliationDepartment of Internal Medicine Botucatu Medical School Sao Paulo State University-
dc.description.affiliationDepartamento de Clinica Medica Faculdade de Medicina de Botucatu UNESP, Rubiao Junior, S/N 18618-970, Botucatu, SP-
dc.description.affiliationFederal University of Mato Grosso Do sul Campo Grande-
dc.description.affiliationDepartment of Morphology Institute of Biosciences Sao Paulo State University-
dc.description.affiliationDepartamento de Morfologia Instituto de Biociencias, Rubiao Junior S/N, Botucatu, SP-
dc.description.affiliationUnespDepartment of Internal Medicine Botucatu Medical School Sao Paulo State University-
dc.description.affiliationUnespDepartamento de Clinica Medica Faculdade de Medicina de Botucatu UNESP, Rubiao Junior, S/N 18618-970, Botucatu, SP-
dc.description.affiliationUnespDepartment of Morphology Institute of Biosciences Sao Paulo State University-
dc.rights.accessRightsAcesso aberto-
dc.relation.ispartofInternational Journal of Cardiology-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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