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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2003.1
- 수록면
- 53 - 59 (7page)
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Tumor target-derived soluble secretary factor has been known to influence macrophage activation to induce nitric oxide (NO) production. Since heme oxigenase-1 (HO-1) is induced by a variety of con-ditions associated with oxidative stress, we ques-tioned whether soluble factor from tumor cels induces HO-1 through NO-dependent mechanism in macrophages. We designated this factor as a because of its ability to activate macrophages to induce iNOS. Although TMAF alone showed mod-est activity, TMAF in combination with IFN-γ signi-ficantly induced iNOS expression and NO syn-thesis. Simultaneously, TMAF induced HO-1 and this induction was slightly augmented by IFN-γ. Surprisingly, however, induction of HO-1 by TMAF was not inhibited by the treatment with the highly selective iNOS inhibitor, 1400 W, indicating that pendent mechanism. While rIFN-γ alone induced iNOS, it had no efect on HO-1 induction by itself. Colectively, the current study reveals that soluble factor from tumor target cells induces HO-1 en-zyme in macrophages. However, overall biological significance of this phenomenon remains to be determined.
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