Soluble factor from tumor cells induces heme oxygenase-1 by a nitric oxide-independent mechanism in murine peritoneal macrophages
Experimental & Molecular Medicine
;
: 53-59, 2003.
Article
in English
| WPRIM
| ID: wpr-78039
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Urinary Bladder Neoplasms
/
Tumor Cells, Cultured
/
Gene Expression Regulation, Enzymologic
/
Cell Line
/
Interferon-gamma
/
Macrophages, Peritoneal
/
Nitric Oxide Synthase
/
Drug Interactions
/
Heme Oxygenase (Decyclizing)
/
Macrophage Activation
Limits:
Animals
/
Humans
Language:
English
Journal:
Experimental & Molecular Medicine
Year:
2003
Type:
Article
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