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Provedor de dados:  56
País:  Brazil
Título:  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
Autores:  Barreto,F.
Rezende,D.C.
Scaramello,C.B.V.
Silva,C.L.M.
Cunha,V.M.N.
Caricati-Neto,A.
Jurkiewicz,A.
Noël,F.
Quintas,L.E.M.
Data:  2010-05-01
Ano:  2010
Palavras-chave:  Α1B-adrenoceptors
Ca2+-ATPases
Cardiac hypertrophy
Na+/K+-ATPase
Mitogen-activated protein kinases
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.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2010000500012
Editor:  Associação Brasileira de Divulgação Científica
Relação:  10.1590/S0100-879X2010007500028
Formato:  text/html
Fonte:  Brazilian Journal of Medical and Biological Research v.43 n.5 2010
Direitos:  info:eu-repo/semantics/openAccess
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