Soluble factor from tumor cells induces heme oxygenase-1 by a nitric oxide-independent mechanism in murine peritoneal macrophages
Exp. mol. med
; Exp. mol. med;: 53-59, 2003.
Article
de En
| WPRIM
| ID: wpr-78039
Bibliothèque responsable:
WPRO
ABSTRACT
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 conditions associated with oxidative stress, we questioned whether soluble factor from tumor cells induces HO-1 through NO-dependent mechanism in macrophages. We designated this factor as a tumor-derived macrophage-activating factor (TMAF), because of its ability to activate macrophages to induce iNOS. Although TMAF alone showed modest activity, TMAF in combination with IFN-gamma significantly induced iNOS expression and NO synthesis. Simultaneously, TMAF induced HO-1 and this induction was slightly augmented by IFN-gamma. Surprisingly, however, induction of HO-1 by TMAF was not inhibited by the treatment with the highly selective iNOS inhibitor, 1400 W, indicating that TMAF induces the HO-1 enzyme by a NO-independent mechanism. While rIFN-gamma alone induced iNOS, it had no effect on HO-1 induction by itself. Collectively, the current study reveals that soluble factor from tumor target cells induces HO-1 enzyme in macrophages. However, overall biological significance of this phenomenon remains to be determined.
Mots clés
Texte intégral:
1
Indice:
WPRIM
Sujet Principal:
Tumeurs de la vessie urinaire
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Cellules cancéreuses en culture
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Régulation de l'expression des gènes codant pour des enzymes
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Lignée cellulaire
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Interféron gamma
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Macrophages péritonéaux
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Nitric oxide synthase
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Interactions médicamenteuses
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Heme oxygenase (decyclizing)
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Activation des macrophages
Limites du sujet:
Animals
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Humans
langue:
En
Texte intégral:
Exp. mol. med
Année:
2003
Type:
Article