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Proliferative response to phenytoin and nifedipine in gingival fibroblasts cultured from humans with gingival fibromatosis
Author(s) -
Sano Masakazu,
Ohuchi Nozomi,
Inoue Tomio,
Tono Kayoko,
Tachikawa Tetsuhiko,
Kizawa Yasuo,
Murakami Hajime
Publication year - 2004
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2004.00257.x
Subject(s) - nifedipine , antagonist , phenytoin , fibromatosis , endocrinology , western blot , receptor , medicine , chemistry , receptor antagonist , endothelin 1 , microbiology and biotechnology , biology , pathology , calcium , biochemistry , epilepsy , neuroscience , gene
The response of gingival fibroblasts cultured from humans with gingival fibromatosis to phenytoin (PHT) and nifedipine (NIF) was investigated. PHT and NIF induced proliferation, and increased the expression of immunoreactive endothelin‐1 (ET‐1). ET‐1 (0.1 n m –1 μ m ) itself also induced proliferation in a concentration‐dependent manner. The proliferation was inhibited by BQ‐123 (ET A receptor antagonist; 1 μ m ) and TAK044 (ET A /ET B receptor antagonist; 1 μ m ), but not by BQ‐788 (ET B receptor antagonist; 1 μ m ). The proliferation induced by PHT (0.25 μ m ) and NIF (0.25 μ m ) was inhibited by BQ‐123 (1 μ m ). In addition, the results of Western blot analysis indicated the presence of ET A and ET B receptors in/on the fibroblasts. These findings suggest that PHT‐ and NIF‐induced gingival proliferation may be mediated by endogenously generated ET‐1, possibly via ET A receptors.