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Type 2 lysophosphatidic acid receptor in gastric surface mucous cells: Possible implication of prostaglandin E 2 production
Author(s) -
Tanaka Tamotsu,
Ohmoto Mayumi,
Morito Katsuya,
Kondo Hiroki,
Urikura Mai,
Satouchi Kiyoshi,
Tokumura Akira
Publication year - 2013
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.1147
Subject(s) - lysophosphatidic acid , chemistry , prostaglandin e , prostaglandin , receptor , gastric acid , production (economics) , microbiology and biotechnology , medicine , biochemistry , stomach , biology , economics , macroeconomics
Lysophosphatidic acid (LPA) is a lipid mediator that induces various cell responses via its specific receptors. Recently, we found that orally administered LPA and phosphatidic acid (PA) ameliorate stress‐ or aspirin‐induced stomach injury. However, the mechanisms underlying these effects have not been elucidated yet. In this study, we examined effect of LPA on prostaglandin (PG) E 2 production in MKN74 cells, a gastric cell‐line expressing type 2 LPA receptor (LPA2). When the cells were treated with LPA, the level of mRNA of COX‐2 but not COX‐1 was upregulated. The LPA effect was abolished when the cells were pretreated with pertussis toxin (PTX), suggesting the involvement of receptor(s) coupled with Gi. Pretreatment of MKN74 cells with LPA enhanced the PGE 2 production triggered by calcium ionophore A23187. Again, PTX abolished the LPA effect. Fluorescent immunohistochemistry using an antibody against LPA2 showed that surface mucous cells (pit cells) in gastric mucosa of mice express LPA2 on the apical side of the plasma membrane. These results suggest that LPA in the diet or its digestion may contribute to the epithelial integrity of stomach mucosa by enhancement of PGE 2 production via activation of LPA2. © 2013 BioFactors, 40(3):355–361, 2014