PT  - JOURNAL ARTICLE
AU  - SANG-JOON PARK
AU  - WON-KEE YOON
AU  - HO-JUN KIM
AU  - HWA-YOUNG SON
AU  - SUNG-WHAN CHO
AU  - KYU-SHIK JEONG
AU  - TAE-HWAN KIM
AU  - SUNG-HO KIM
AU  - SE-RA KIM
AU  - SI-YUN RYU
TI  - 2,3,7,8-Tetrachlorodibenzo-p-dioxin Activates ERK and p38 Mitogen-activated Protein Kinases in RAW 264.7 Cells
DP  - 2005 Jul 01
TA  - Anticancer Research
PG  - 2831--2836
VI  - 25
IP  - 4
4099  - http://ar.iiarjournals.org/content/25/4/2831.short
4100  - http://ar.iiarjournals.org/content/25/4/2831.full
SO  - Anticancer Res2005 Jul 01; 25
AB  - 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. Copyright© 2005 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved