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β‐Adrenergic‐induced CD40 overexpression on gingival fibroblasts: Role of PGE 2
Author(s) -
Furlán César,
SterinBorda Leonor,
Borda Enri
Publication year - 2010
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1042/cbi20090028
Subject(s) - prostaglandin e2 , fibroblast , haematopoiesis , prostaglandin e , chemistry , receptor , cd40 , prostaglandin , endocrinology , mediator , agonist , microbiology and biotechnology , medicine , stimulation , cell culture , biology , stem cell , biochemistry , in vitro , cytotoxic t cell , genetics
CD40, a member of the tumour necrosis factor‐α receptor family, is constitutively expressed by cells of haematopoietic and non‐haematopoietic origin, including fibroblasts. Signalling through this receptor molecule regulates inflammatory mediator secretion by many cell types. The work has been performed in healthy subjects and the authors studied, by cellular culture, flow cytometric analysis and ELISA assay, the expression of CD40 and PGE 2 (prostaglandin E 2 ) generation on gingival fibroblasts stimulated by β‐AR (β‐adrenoceptor) agonists. Herein, the authors demonstrate that β‐AR subtype activation via their own specific agonists markedly increased CD40 expression on human gingival fibroblasts. This effect was prevented by β‐AR subtype‐specific antagonists. In addition, gingival fibroblast β‐AR stimulation resulted in an increase in PGE 2 generation. The inhibition of PLA 2 (phospholipase A 2 ) and COX‐1 (cyclo‐oxygenase‐1) but not COX‐2 impaired β‐AR increase of PGE 2 , an effect that was restored by the addition of low concentrations of PGE 2 , suggesting that PGE 2 generation is implicated in the mechanism underlying β‐AR‐agonist‐mediated CD40 overexpression. Our work has revealed an endogenous β‐AR mediator network involving gingival fibroblasts.