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Nicotine and platelet activating factor (PAF) in hyperplasia of human gingival fibroblasts: Possible roles in periodontal disease.


Description

Objective. To determine a mechanism by which nicotine and platelet activating factor (PAF) induce human gingival fibroblast proliferation resulting in periodontal diseases. Methods. Human gingival fibroblasts were cultured and stimulated with 1--100muM and 1--100 mM concentrations of nicotine with and without 10nM PAF for different time points. Treatment with inflammatory agents (LPS, TNF-alpha, TGF-alpha, HETES, IL-6, IL-8 and LTD4) were also examined. Cell proliferation, protein expression and PAF-receptor binding were measured by 3H-Thymidine incorporation, western blotting and 3H-PAF to receptor complexes scintillation spectrophotometry, respectively. Results. Data show that (1) Nicotine and PAF induce MAPK, alpha-SMA, Bcl-2 and Bax protein expressions; (2) cGMP inhibits proliferation; and (3) inflammatory mediators modulate PAF responses. Conclusions. These findings collectively highlight cGMP as a novel mechanism for inhibiting the effect nicotine and PAF have on fibroblasts. It may regulate fibroblast signaling and proliferation and therefore, the severity of inflammation.