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Department of Health Chemistry, School of Pharmaceutical Sciences, Showa University, Hatanodai, Shinagawa-ku, Tokyo, Japan
Mast cells exhibit a biphasic (immediate and delayed)
eicosanoid-biosynthetic response after stimulation with particular
cytokines or Fc
RI (high affinity receptor for IgE) cross-linking.
Treatment of rat serosal connective tissue mast cells (CTMC) with nerve
growth factor (NGF) induced only the delayed phase of PGD2
generation that depended on inducible cyclooxygenase-2 (COX-2), but not
constitutive COX-1, even though the subcellular distributions of these
isoforms were similar. Experiments using several phospholipase
A2 (PLA2) isozyme-specific probes and
inhibitors suggested that both constitutive cytosolic PLA2
and inducible type IIA secretory PLA2 (sPLA2)
are involved in NGF-initiated, COX-2-dependent, delayed
PGD2 generation in rat CTMC. A type IIA sPLA2
inhibitor, but neither cytosolic PLA2 nor COX inhibitors,
reduced, while adding exogenous type IIA sPLA2 augmented,
NGF-induced COX-2 expression and its attendant PGD2
generation, indicating that the sPLA2-mediated increase in
delayed PGD2 generation was attributable mainly to enhanced
COX-2 expression. Type IIA sPLA2 and its close relative
type V sPLA2 associated with fibroblastic cell surfaces
increased NGF-induced COX-2 expression more efficiently than the
soluble enzymes, revealing a particular juxtacrine sPLA2
presentation route. Surprisingly, catalytically inactive type IIA
sPLA2 mutants, which were incapable of promoting
arachidonic acid release from cytokine-primed cells, retained the
ability to enhance COX-2 expression in CTMC, indicating that the
COX-2-inducing activities of sPLA2 are independent of their
catalytic functions.
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