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J. Biol. Chem., Vol. 275, Issue 51, 40028-40035, December 22, 2000
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From the School of Pharmaceutical Sciences, Kitasato University,
5-9-1 Shirokane, Minato-ku, Tokyo 108-8641, Japan
Antigenic cross-linking of the high affinity IgE
receptors on mast cells induced the synthesis of prostaglandin
D2 (PGD2). The production of
PGD2 in L9 cells, which overexpressed non-mitochondrial phospholipid glutathione peroxidase (PHGPx), was only one-third that in
the control line of cells (S1 cells). The reduction in the formation of
PGD2 in L9 cells was reversed upon inhibition of PHGPx
activity by buthionine sulfoximine. Experiments with inhibitors
demonstrated that prostaglandin H synthase-2 (PGHS-2) was the isozyme
responsible for the production of PGD2 upon cross-linking of IgE receptors. The conversion of radiolabeled arachidonic acid to
prostaglandin H2 (PGH2) was strongly inhibited
in L9 cells, whereas the rate of conversion of PGH2 to
PGD2 was the same in L9 cells and S1 cells, indicating that
PGHS was inactivated in L9 cells. The PGHS activity in L9 cells
was about half that in S1 cells. However, PGHS activity in L9 cells
increased to the level in S1 cells upon the addition of the
hydroperoxide 15-hydroperoxyeicosatetraenoic acid or of
3-chloroperoxybenzoic acid. These results suggest that non-mitochondrial PHGPx might be involved in the inactivation of PGHS-2
in nucleus and endoplasmic reticulum via reductions in levels of the
hydroperoxides that are required for full activation of PGHS.
Therefore, it appears that PHGPx might function as a modulator of the
production of prostanoids, in addition to its role as an antioxidant enzyme.
Involvement of Phospholipid Hydroperoxide Glutathione Peroxidase
in the Modulation of Prostaglandin D2 Synthesis*
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed. Tel./Fax:
81-3-3444-4943; E-mail: nakagaway@pharm.kitasato-u.ac.jp.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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