Open Access2,3,7,8‐Tetrachlorodibenzo‐p‐dioxin (TCDD)‐Induced Activation of Mitogen‐Activated Protein Kinase Signaling Pathway in Jurkat T Cells
Author(s) -
Kwon MyungJa,
Jeong KyuShik,
Choi Eun Jeong,
Lee Byung Ho
Publication year - 2003
Publication title -
pharmacology & toxicology
Language(s) - English
Resource type - Journals
eISSN - 1600-0773
pISSN - 0901-9928
DOI - 10.1034/j.1600-0773.2003.930406.x
Subject(s) - jurkat cells , mapk/erk pathway , protein kinase a , kinase , p38 mitogen activated protein kinases , viability assay , ask1 , mitogen activated protein kinase , signal transduction , microbiology and biotechnology , apoptosis , mitogen activated protein kinase kinase , biology , chemistry , immunology , biochemistry , t cell , immune system
Abstract: The present study was performed to examine mitogen‐activated protein kinase associated pathways in mediation of 2,3,7,8‐tetrachlorodibenzo‐ p ‐dioxin (TCDD)‐induced cell apoptosis in cultured Jurkat T cells. TCDD significantly decreased cell viability in a concentration‐dependent manner (P<0.05 at 10–300 nM). TCDD (10 nM) also time‐dependently decreased cell viability (P<0.05 at 12–48 hr). c‐Jun NH 2 ‐terminal kinase was significantly phosphorylated with TCDD treatment in a time dependent manner. p38 Mitogen‐activated protein kinase was not significantly changed with TCDD treatment. Extracellular signal‐regulated protein kinase was significantly phosphorylated with TCDD treatment for 8 hr and gradually returned to baseline. TCDD induced up‐regulation of ASK1 and C‐Jun, which are up‐ and down‐stream of JNK, respectively, and up‐regulation of cytosolic cytochrome c and caspase‐3. These results demonstrate that MAPK signaling pathways including JNK and ERK 1/2, are activated with the treatment of TCDD in Jurkat T cells, which suggest that MAPK pathways may be involved in TCDD‐induced cell death.