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Prostaglandin F 2α upregulates intercellular adhesion molecule‐1 expression in human gingival fibroblasts
Author(s) -
Noguchi Kazuyuki,
Iwasaki Kengo,
Ishikawa Isao
Publication year - 1999
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1999.tb02254.x
Subject(s) - intercellular adhesion molecule 1 , intracellular , adhesion , microbiology and biotechnology , chemistry , cell adhesion molecule , prostaglandin e2 , prostaglandin , prostaglandin e , biology , biochemistry , endocrinology , organic chemistry
Prostaglandin F 2α (PGF 2α ) is a bioactive lipid mediator, which has been suggested to be involved in the pathogenesis of periodontal disease. However, the roles of PGF 2α in the disease are not well understood. In the present study, we investigated the effect of PGF 2α on intercellular adhesion molecule‐1 (ICAM‐1) expression in human gingival fibroblasts (HGF) and the effect of PGF 2α on ICAM‐1 expression elicited by proinflammatory cytokines, interferon‐γ (IFN‐γ) and tumour necrosis factor α (TNFα) in the cells. PGF 2α ‐stimulated HGF expressed ICAM‐1 expression in a time‐ and dose‐dependent manner. IFN‐γ‐elicited ICAM‐1 expression was synergistically increased by PGF 2α whereas TNFα‐induced ICAM‐1 expression was slightly inhibited by PGF 2α . Fluprostenol, a selective FP receptor agonist, could mimic PGF 2α ‐induced effect on ICAM‐1 expression. Furthermore, signal transduction for the regulation of ICAM‐1 by PGF 2α was investigated using N‐(6‐aminohexyl)‐5‐chloro‐1‐naphthalenesulphonamide (W‐7), a calcium calmodulin antagonist, and l‐(5‐isoquinolinylsulphonyl)‐2‐methylpiperazine (H‐7), an inhibitor of protein kinase C (PKC). W‐7 and H‐7, remarkably, suppressed PGF 2α ‐induced ICAM‐1 expression and synergistic increase of ICAM‐1 expression by combination of PGF 2α and IFN‐γ, while IFN‐γ‐elicited ICAM‐1 expression was only partially inhibited by W‐7 and H‐7. From these data, we suggest that PGF 2α upregulates ICAM‐1 expression in HGF and synergistically enhances IFN‐γ‐induced ICAM‐1 expression through FP receptor by calcium calmodulin‐dependent and PKC‐dependent pathways. PGF 2α may be involved in the pathology of periodontal disease by upregulating ICAM‐1 expression in HGF.