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J. Biol. Chem., Vol. 279, Issue 47, 48923-48929, November 19, 2004

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MITF Is Necessary for Generation of Prostaglandin D₂ in Mouse Mast Cells^*

Eiichi Morii and Keisuke Oboki

From the Department of Pathology, Osaka University Medical School, Suita, Osaka 565-0871, Japan

Mast cells generate eicosanoids that are linked to asthma and other inflammatory diseases. A basic-helix-loop-helix leucine zipper transcription factor termed MITF is essential for the development of mast cells. Although other substances also linked to inflammatory reactions (such as various proteases and serotonin) require MITF for their expression, the role of MITF in eicosanoid generation has not been studied. We examined eicosanoid generation in bone marrow-derived mast cells (BMMCs) of tg/tg mice that lack MITF. Most eicosanoids generated by BMMCs are either prostaglandin (PG) D₂ or leukotriene C₄. The former is synthesized via the cyclooxygenase pathway, whereas the latter is synthesized via the 5-lipoxygenase pathway. In response to stimulation with IgE and antigens, BMMCs of tg/tg mice synthesized leukotriene C₄ normally. However, neither immediate nor delayed PGD₂ production was detected in these BMMCs. This indicates that MITF is a transcription factor that specifically activates the cyclooxygenase pathway, but not the 5-lipoxygenase pathway. Significant decreases in expression of hematopoietic PGD₂ synthase (hPGDS, a terminal synthase for PGD₂) were observed at both mRNA and protein levels in tg/tg BMMCs. MITF transactivated the hPGDS gene via a CACCTG motif located in the promoter region. MITF appeared to be essential for generation of PGD₂ by enhancing expression of the hPGDS gene in BMMCs.

Received for publication, June 23, 2004 , and in revised form, September 10, 2004.

^* This work was supported by grants from the Ministry of Education, Culture, Sports, Science, and Technology, Japan and the Osaka Cancer Society. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Present address: Research Unit for Allergy Transcriptome, RIKEN Yokohame Institute, Yokohame, Kanagawa 230-0045, Japan.

To whom correspondence should be addressed: Dept. of Pathology, Rm. C2, Osaka University Medical School, Yamada-oka 2–2, Suita 565-0871, Japan. Tel.: 81-6-6879-3721; Fax: 81-6-6879-3729; E-mail: morii{at}patho.med.osaka-u.ac.jp.

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