Activation of calcium-sensing receptors is associated with apoptosis in cardiomyocytes under simulated ischemia/reperfusion / 浙江大学学报·医学版
Journal of Zhejiang University. Medical sciences
; (6): 207-212, 2011.
Artigo
em Chinês
| WPRIM (Pacífico Ocidental)
| ID: wpr-319808
Biblioteca responsável:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To examine the association of activation of calcium-sensing receptors (CaSR) with apoptosis in cardiomyocytes under simulated ischemia/reperfusion.</p><p><b>METHODS</b>Ventricular cardiomyocytes of neonatal rats were incubated in ischemia-mimetic solution for 2 h, then re-incubated in normal culture medium for 24 h to establish a model of simulated ischemia/reperfusion (I/R). Cell apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL assay). The expression of CaSR mRNA was detected by reverse transcriptase polymerase chain reaction (RT-PCR). The expression of Caspase -3 and Bcl-2 was detected by Western blotting.</p><p><b>RESULT</b>The simulated I/R enhanced the expression of CaSR and cardiomyocyte apoptosis. GdCl(3), a specific activator of CaSR, further increased the expression of CaSR and cardiomyocyte apoptosis, along with upregulation of Caspase-3 and downregulation of Bcl-2.</p><p><b>CONCLUSION</b>CaSR is associated with I/R injury and apoptosis in neonatal rat ventricular cardiomyocytes via suppressing Bcl-2 and promoting Caspase -3 expression.</p>
Texto completo:
Disponível
Contexto em Saúde:
ODS3 - Meta 3.4 Reduzir as mortes prematuras devido doenças não transmissíveis
Problema de saúde:
Doença Cardiovascular
/
Doença Isquêmica do Coração
Base de dados:
WPRIM (Pacífico Ocidental)
Assunto principal:
Patologia
/
Fisiologia
/
Traumatismo por Reperfusão Miocárdica
/
Transdução de Sinais
/
Células Cultivadas
/
Apoptose
/
Proteínas Proto-Oncogênicas c-bcl-2
/
Miócitos Cardíacos
/
Receptores de Detecção de Cálcio
/
Caspase 3
Limite:
Animais
Idioma:
Chinês
Revista:
Journal of Zhejiang University. Medical sciences
Ano de publicação:
2011
Tipo de documento:
Artigo