2,3,7,8-Tetrachlorodibenzo-p-dioxin activates ERK and p38 mitogen-activated protein kinases in RAW 264.7 cells.
Anticancer Res
; 25(4): 2831-6, 2005.
Article
en En
| MEDLINE
| ID: mdl-16080534
ABSTRACT
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental contaminant, exposure to it eliciting a broad spectrum of deleterious pathophysiological effects. Since mitogen-activated protein kinase (MAPK) pathways appear to play an important role in both cell survival and the apoptotic process, we assessed the effects of TCDD on the activation of extracellular signal-regulated kinase (ERK), Jun-N-terminal kinase (JNK), p38 MAPKs and caspase-3 in RAW 264.7 cells. TCDD treatment induced a transient upshift in ERK activity, followed by a decline, but a concomitant dramatic activation of p38. However, TCDD did not cause any apparent change in the activity of JNK, though it induced an up-regulation in caspase-3 activity. These results demonstrate that the equilibrium between the ERK and p38 pathways is critical to the fate of the cells, and that the activation of p38, upstream of caspase, plays an important role in the apoptotic process. The data obtained in this study also suggests that TCDD activates the MAPK pathway via an arylhydrocarbon receptor (AhR)-independent mechanism in RAW 264.7 murine macrophages.
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Banco de datos:
MEDLINE
Asunto principal:
Quinasas MAP Reguladas por Señal Extracelular
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Proteínas Quinasas JNK Activadas por Mitógenos
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Proteínas Quinasas p38 Activadas por Mitógenos
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Dibenzodioxinas Policloradas
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Macrófagos
Límite:
Animals
Idioma:
En
Año:
2005
Tipo del documento:
Article