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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2003.1
- 수록면
- 431 - 437 (7page)
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초록· 키워드
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TNF-α, a trimeric cytokine, was known to inhibit diferention of preadipocytes to adipocytes. In the present study, we investigated signal mediators working downstream of TNF-α using murine 3T3- L1 cells. TNF-α induced activation of both c-jun NH2-terminal kinase (JNK) and nuclear trans-cription factor-κB (NF-κB) in 3T3-L1 cells. Block-age of these two mediators activities by specific inhibitors, SP600125 and Ad-IκBα-SR restored adi-pogenesis diferentiation suggesting their involve-cels by TNF-α. Consistent with previous studies, peroxisome proliferator-activated receptor gama (PPARγ) a key transcriptional regulator was re-markably reduced by TNF-α treatment. Compared with adipogenesis, however, SP600125, a chemi-cal JNK inhibitor hardly relieved TNF-α effect on PPARγ expression whereas S32A/S36A mutant of IκBα considerably recovered PPARγ expression, indicating that two signal mediators exploit separ-sis. These results sugest that inhibition of 3T3- L1 cels diferentiation by TNF-α is partly imple-mented through NF-κB and one of its downstream effectors be PARγ.
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