Lack of evidence for regulation of cardiac P-type ATPases and MAP kinases in transgenic mice with cardiac-specific overexpression of constitutively active α1B-adrenoceptors

Lack of evidence for regulation of cardiac P-type ATPases and MAP kinases in transgenic mice with cardiac-specific overexpression of constitutively active α1B-adrenoceptors

Autor Barreto, Frederico Google Scholar
Rezende, Daniele Campos Google Scholar
Scaramello, Christianne Bretas Vieira Google Scholar
Silva, Claudia Lucia Martins Google Scholar
Cunha, Valeria do Monti Nascimento Google Scholar
Caricati-Neto, Afonso Autor UNIFESP Google Scholar
Jurkiewicz, Aron Autor UNIFESP Google Scholar
Noël, Francois Google Scholar
Quintas, Luis Eduardo Menezes Google Scholar
Instituição Universidade Federal do Rio de Janeiro Instituto de Ciências Biomédicas Programa de Farmacologia
Universidade Federal Fluminense Instituto Biomédico Departamento de Fisiologia e Farmacologia
Universidade Federal de São Paulo (UNIFESP)
Resumo The regulatory function of α1B-adrenoceptors in mammalian heart homeostasis is controversial. The objective of the present study was to characterize the expression/activity of key proteins implicated in cardiac calcium handling (Na+/K+-ATPase and Ca2+-ATPases) and growth (ERK1/2, JNK1/2 and p38) in mice with cardiac-selective overexpression of constitutively active mutant α1B-adrenoceptor (CAMα1B-AR), which present a mild cardiac hypertrophy phenotype. Immunoblot assays showed that myocardial plasma membrane Ca2+-ATPase (PMCA) expression was increased by 30% in CAMα1B-AR mice (N = 6, P < 0.05), although there was no change in sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2) expression. Moreover, total Ca2+-ATPase activity was not modified, but a significant increase in the activity of the thapsigargin-resistant (PMCA) to thapsigargin-sensitive (SERCA) ratio was detected. Neither Na+/K+-ATPase activity nor the expression of α1 and α2 subunit isoforms was changed in CAMα1B-AR mouse hearts. Moreover, immunoblot assays did not provide evidence for an enhanced activation of the three mitogen-activated protein kinases studied in this stage of hypertrophy. Therefore, these findings indicate that chronic cardiac α1B-AR activation in vivo led to mild hypertrophy devoid of significant signs of adaptive modifications concerning primary intracellular calcium control and growth-related proteins, suggesting a minor pathophysiological role of this adrenergic receptor in mouse heart at this stage of development.
Palavra-chave α1B-adrenoceptors
Ca2+-ATPases
Cardiac hypertrophy
Na+/K+-ATPase
Mitogen-activated protein kinases
Idioma Inglês
Financiador Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Data de publicação 2010-05-01
Publicado em Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 43, n. 5, p. 500-505, 2010.
ISSN 0100-879X (Sherpa/Romeo, fator de impacto)
Publicador Associação Brasileira de Divulgação Científica
Extensão 500-505
Fonte http://dx.doi.org/10.1590/S0100-879X2010007500028
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000277830900012
SciELO S0100-879X2010000500012 (estatísticas na SciELO)
Endereço permanente http://repositorio.unifesp.br/handle/11600/5700

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