2,3,7,8-Tetrachlorodibenzo-p-dioxin Activates ERK and p38 Mitogen-activated Protein Kinases in RAW 264.7 Cells
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 p...
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Published in | Anticancer research Vol. 25; no. 4; pp. 2831 - 2836 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Attiki
International Institute of Anticancer Research
01.07.2005
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Subjects | |
Online Access | Get full text |
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Summary: | 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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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0250-7005 1791-7530 |