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Different roles of ERK(1/2) and p38 MAPK(alpha/beta) in cellular signaling during cardiomyocyte anoxia preconditioning / 生理学报
Acta Physiologica Sinica ; (6): 454-458, 2003.
Artigo em Chinês | WPRIM | ID: wpr-290944
ABSTRACT
Preconditioning (PC) exhibits earlier and delayed protection. But the mechanism of cellular signaling in delayed protection of PC remains unclear. We explored the roles of ERK(1/2) and p38 MAPK(alpha/beta) (p38(alpha/beta)) in delayed protection of anoxia preconditioning (APC). The anoxia/reoxygenation (A/R) injury and APC models were established in cultured neonatal rat cardiomyocytes. An ERK(1/2) inhibitor (PD98059) and a p38(alpha/beta) blocker (SB203580) were applied and their effects on A/R and APC models were observed. The cellular contents of MDA, SOD, cell viability and LDH release was measured at the end of the study. ERK(1/2) and p38 MAPK total activity was measured by in-gel myelin basic protein phosphorylation assay at different points during sustained anoxia. The results obtained are as follows (1) PD98059 (but not SB203580), administered in preconditioning anoxia phase in APC group, abolished completely the delayed protection of APC; (2) SB203580 administered in sustained anoxia phase in A/R group could relieve cell injury induced by anoxia, but not by PD98059; (3) the highest activity of ERK(1/2) and p38 MAPK induced by anoxia appeared at 4 h after the beginning of sustained anoxia. APC inhibited the over activation of both ERK(1/2) and p38 during the following sustained anoxia. These results suggest that ERK(1/2) activation during preconditioning may be an important link of cell signal transduction in the mechanism of APC delayed protection. p38(alpha/beta) activation at the preconditioning stage dose not participate in signaling of APC delayed protection. The excessive activation of p38(alpha/beta) is possibly a key factor in mediating cell injury induced by sustained anoxia. The inhibition of p38(alpha/beta) excessive activation during subsequent sustained anoxia might play a role in delayed protection mechanism of APC.
Assuntos
Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Fisiologia / Transdução de Sinais / Hipóxia Celular / Células Cultivadas / Ratos Sprague-Dawley / Precondicionamento Isquêmico Miocárdico / Proteína Quinase 1 Ativada por Mitógeno / Biologia Celular / Miócitos Cardíacos / MAP Quinases Reguladas por Sinal Extracelular Tipo de estudo: Estudo prognóstico Limite: Animais Idioma: Chinês Revista: Acta Physiologica Sinica Ano de publicação: 2003 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Fisiologia / Transdução de Sinais / Hipóxia Celular / Células Cultivadas / Ratos Sprague-Dawley / Precondicionamento Isquêmico Miocárdico / Proteína Quinase 1 Ativada por Mitógeno / Biologia Celular / Miócitos Cardíacos / MAP Quinases Reguladas por Sinal Extracelular Tipo de estudo: Estudo prognóstico Limite: Animais Idioma: Chinês Revista: Acta Physiologica Sinica Ano de publicação: 2003 Tipo de documento: Artigo