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Cyclosporin A upregulates prostaglandin E 2 production in human gingival fibroblasts challenged with tumor necrosis factor alpha in vitro
Author(s) -
Wondimu Biniyam,
Modéer Thomas
Publication year - 1997
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.1997.tb00003.x
Subject(s) - tumor necrosis factor alpha , prostaglandin e , prostaglandin e2 , endocrinology , in vitro , prostaglandin , cyclooxygenase , chemistry , arachidonic acid , medicine , pathogenesis , pharmacology , biochemistry , enzyme
The effect of Cyclosporin A (CsA) on prostaglandin E 2 (PGE 2 ) production in human gingival fibroblasts challenged with tumor necrosis factor alpha (TNF‐α) was studied. TNF‐α (1‐100 ng/ml) dose‐dependently stimulated PGE 2 ; formation in 24 h cultures. CsA (1‐100 ng/ml) did not induce PGE 2 ; formation itself but potentiated TNF‐α induced PGE; formation in gingival fibroblasts in a manner dependent on the concentrations of both CsA and TNF‐α. TNF‐α (10 ng/ml) stimulated the release of [ 3 H]‐arachidonic acid (A.A) from prelabelled fibroblasts that was potentiated by CsA (100 ng/ml). Addition of exogenous unlabelled AA (5‐20 μM/ml) to the cells resulted in enhanced PGE 2 : formation that was not potentiated by CsA (100 ng/mi). Furthermore. CsA (100 ng/ml) did not further increase the level of cyclooxygenase‐2 mRNA induced by TNF‐α (10 ng/ml). although PGE 2 formation was enhanced. The results indicate that CsA and TNF‐α act in concert on PGE 2 formation in gingival fibroblasts. which may be of importance in the pathogenesis of gingival overgrowth induced by the drug.