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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Voltarelli, Vanessa A. [1] ; Bechara, Luiz R. G. [1] ; Bacurau, Aline V. N. [1] ; Mattos, Katt C. [1] ; Dourado, Paulo M. M. [2] ; Bueno, Jr., Carlos R. [3] ; Casarini, Dulce E. [4] ; Negrao, Carlos E. [1, 2] ; Brum, Patricia C. [1]
Total Authors: 9
[1] Univ Sao Paulo, Escola Educ Fis & Esporte, BR-05508900 Sao Paulo - Brazil
[2] Univ Sao Paulo, Fac Med, Inst Heart, BR-05508900 Sao Paulo - Brazil
[3] Univ Sao Paulo, Sch Phys Educ & Sport, BR-14049 Ribeirao Preto - Brazil
[4] Univ Fed Sao Paulo, Dept Med, Div Nephrol, Sao Paulo - Brazil
Total Affiliations: 4
Document type: Journal article
Source: JOURNAL OF CELLULAR AND MOLECULAR MEDICINE; v. 18, n. 6, p. 1087-1097, JUN 2014.
Web of Science Citations: 10

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. (AU)

FAPESP's process: 08/56483-1 - Role of B2-adrenergic receptors in skeletal muscle disorders triggered by heart failure
Grantee:Vanessa Azevedo Voltarelli
Support type: Scholarships in Brazil - Master
FAPESP's process: 10/50048-1 - Cellular and functional bases of exercise in cardiovascular diseases
Grantee:Carlos Eduardo Negrão
Support type: Research Projects - Thematic Grants