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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2007.1
- 수록면
- 524 - 534 (11page)
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초록· 키워드
오류제보하기
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a proto-typic halogenated aromatic hydrocarbon (HAH), is part of its toxic effects appears to be derived from its ability to induce TNF-α production. However, the sig-naling pathway of TCDD that leads to TNF-α ex-pression has not been elucidated. In this study, we in-vestigated the signaling mechanism of TCD-induced TNF-α expression in PMA-differentiated THP-1 macrophages. TCDD induced both mRNA and protein expression of TNF-α in a dose- and time-dependent manner. αreceptor (AhR) inhibitor, prevented the TCDD-induced expression of TNF-α at both mRNA and protein levels. Genistein, a protein tyrosine kinase (PTK) inhibitor, and PD153035, an EGFR inhibitor, also blocked the in-crease of TNF-α expression by TCDD, indicating the role of EGFR in TCDD-induced TNF-α expression. On the other hand, P2, a c-Src specific inhibitor, did not affect TCDD-induced TNF-α expression. EGFR phos-treatment. TCDD-induced EGFR activation was AhR-dependent since co-treatment with α-NF pre-vented it. ERK was found to be a downstream efector of EGFR activation in the signaling pathway leading to TNF-α production after TCDD stimulation. Activation of ERK was observed from 30 min after TCDD treatment. PD98059, an inhibitor of the MEK-ERK path-way, completely prevented the TNF-α mRNA and pro-tein expression induced by TCDD, whereas inhibitors EGFR inhibitor, as well as α-NF significantly reduced ERK phosphorylation, suggesting that ERK activation by TCDD was mediated by both EGFR and AhR. These results indicate that TNF-α production by TCDD in dif-ferentiated THP-1 macrophages is AhR-dependent and involves activation of EGFR and ERK, but not c-Src, JNK, nor p38 MAPK. A signaling pathway is pro-posed where TCDD induces sequential activation of AhR, EGFR and ERK, leading to the increased ex-pression of TNF-α.
목차
등록된 정보가 없습니다.
참고문헌 (21)
참고문헌 신청
Ahmed S / 2005 / Protein kinase Ctheta activity is involved in the 2,3,7,8-tetrachloro-dibenzo-p-dioxin-induced signal transduction pathway leading to apoptosis in L-MAT, a h
Brewster DW / / causes an increase in protein kinases particularly protein kinase C in the hepatic plasma membrane of the rat and the guinea pig : 8 296 ~ 302
Chin BY / 1998 / Induction of apoptosis by particulate matter: role of TNF-alpha and MAPK 275 : L942 ~ L949
Clark GC / / Tumor necrosis factor involvement in 2 8-tetrachlorodibenzo- p-dioxin-mediated endotoxin hypersensitivity in C57BL/6J mice congenic at the Ah locus : 422 ~ 31
Davis JW / 2003 / The aryl hydrocarbon receptor antagonist, 3'methoxy-4'nitroflavone, attenuates 2,3,7,8-tetrachlorodibenzo-p-dioxin-dependent regulation of growth factor sig
Brewster DW / / causes an increase in protein kinases particularly protein kinase C in the hepatic plasma membrane of the rat and the guinea pig : 8 296 ~ 302
Chin BY / 1998 / Induction of apoptosis by particulate matter: role of TNF-alpha and MAPK 275 : L942 ~ L949
Clark GC / / Tumor necrosis factor involvement in 2 8-tetrachlorodibenzo- p-dioxin-mediated endotoxin hypersensitivity in C57BL/6J mice congenic at the Ah locus : 422 ~ 31
Davis JW / 2003 / The aryl hydrocarbon receptor antagonist, 3'methoxy-4'nitroflavone, attenuates 2,3,7,8-tetrachlorodibenzo-p-dioxin-dependent regulation of growth factor sig
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