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Evidence that PAR2‐triggered prostaglandin E 2 (PGE 2 ) formation involves the ERK‐cytosolic phospholipase A 2 ‐COX‐1‐microsomal PGE synthase‐1 cascade in human lung epithelial cells
Author(s) -
Nagataki Mami,
Moriyuki Kazumi,
Sekiguchi Fumiko,
Kawabata Atsufumi
Publication year - 2008
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1434
Subject(s) - phospholipase a2 , prostaglandin , prostaglandin e , cytosol , phospholipase a , stimulation , microsome , receptor , isozyme , prostaglandin e2 , mapk/erk pathway , enzyme , phospholipase c , atp synthase , chemistry , eicosanoid , endocrinology , biology , medicine , kinase , biochemistry , arachidonic acid
Abstract We investigated possible involvement of three isozymes of prostaglandin E synthase (PGES), microsomal PGES‐1 (mPGES‐1), mPGES‐2 and cytosolic PGES (cPGES) in COX‐2‐dependent prostaglandin E 2 (PGE 2 ) formation following proteinase‐activated receptor‐2 (PAR2) stimulation in human lung epithelial cells. PAR2 stimulation up‐regulated mPGES‐1 as well as COX‐2, but not mPGES‐2 or cPGES, leading to PGE 2 formation. The PAR2‐triggered up‐regulation of mPGES‐1 was suppressed by inhibitors of COX‐1, cytosolic phospholipase A 2 (cPLA 2 ) and MEK, but not COX‐2. Finally, a selective inhibitor of mPGES‐1 strongly suppressed the PAR2‐evoked PGE 2 formation. PAR2 thus appears to trigger specific up‐regulation of mPGES‐1 that is dependent on prostanoids formed via the MEK/ERK/cPLA 2 /COX‐1 pathway, being critical for PGE 2 formation. Copyright © 2007 John Wiley & Sons, Ltd.

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