Lack of beta(2)-adrenoceptors aggravates heart failure-induced skeletal muscle myopathy in mice

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dc.contributor.author Voltarelli, Vanessa A.
dc.contributor.author Bechara, Luiz R. G.
dc.contributor.author Bacurau, Aline V. N.
dc.contributor.author Mattos, Katt C.
dc.contributor.author Dourado, Paulo M. M.
dc.contributor.author Bueno, Carlos R.
dc.contributor.author Casarini, Dulce E. [UNIFESP]
dc.contributor.author Negrao, Carlos E.
dc.contributor.author Brum, Patricia C.
dc.date.accessioned 2016-01-24T14:37:20Z
dc.date.available 2016-01-24T14:37:20Z
dc.date.issued 2014-06-01
dc.identifier http://dx.doi.org/10.1111/jcmm.12253
dc.identifier.citation Journal of Cellular and Molecular Medicine. Hoboken: Wiley-Blackwell, v. 18, n. 6, p. 1087-1097, 2014.
dc.identifier.issn 1582-4934
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/37795
dc.description.abstract Skeletal myopathy is a hallmark of heart failure (HF) and has been associated with a poor prognosis. HF and other chronic degenerative diseases share a common feature of a stressed system: sympathetic hyperactivity. Although beneficial acutely, chronic sympathetic hyperactivity is one of the main triggers of skeletal myopathy in HF. Considering that (2)-adrenoceptors mediate the activity of sympathetic nervous system in skeletal muscle, we presently evaluated the contribution of (2)-adrenoceptors for the morphofunctional alterations in skeletal muscle and also for exercise intolerance induced by HF. Male WT and (2)-adrenoceptor knockout mice on a FVB genetic background (2KO) were submitted to myocardial infarction (MI) or SHAM surgery. Ninety days after MI both WT and 2KO mice presented to cardiac dysfunction and remodelling accompanied by significantly increased norepinephrine and epinephrine plasma levels, exercise intolerance, changes towards more glycolytic fibres and vascular rarefaction in plantaris muscle. However, 2KO MI mice displayed more pronounced exercise intolerance and skeletal myopathy when compared to WT MI mice. Skeletal muscle atrophy of infarcted 2KO mice was paralleled by reduced levels of phosphorylated Akt at Ser 473 while increased levels of proteins related with the ubiquitin--proteasome system, and increased 26S proteasome activity. Taken together, our results suggest that lack of (2)-adrenoceptors worsen and/or anticipate the skeletal myopathy observed in HF. en
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent 1087-1097
dc.language.iso eng
dc.publisher Wiley-Blackwell
dc.relation.ispartof Journal of Cellular and Molecular Medicine
dc.rights Acesso aberto
dc.subject heart failure en
dc.subject skeletal muscle en
dc.subject (2)-adrenoceptors en
dc.subject proteasome en
dc.title Lack of beta(2)-adrenoceptors aggravates heart failure-induced skeletal muscle myopathy in mice en
dc.type Artigo
dc.rights.license http://olabout.wiley.com/WileyCDA/Section/id-406071.html
dc.contributor.institution Universidade de São Paulo (USP)
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Univ São Paulo, Escola Educ Fis & Esporte, BR-05508900 São Paulo, Brazil
dc.description.affiliation Univ São Paulo, Fac Med, Inst Heart, BR-05508900 São Paulo, Brazil
dc.description.affiliation Univ São Paulo, Sch Phys Educ & Sport, BR-14049 Ribeirao Preto, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Med, Div Nephrol, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Med, Div Nephrol, São Paulo, Brazil
dc.description.sponsorshipID FAPESP: 2008/56483-1
dc.description.sponsorshipID CNPq: 302201/2011-4
dc.description.sponsorshipID FAPESP: 2010/50048-1
dc.identifier.file WOS000340390500014.pdf
dc.identifier.doi 10.1111/jcmm.12253
dc.description.source Web of Science
dc.identifier.wos WOS:000340390500014



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