ISSN:
1600-0765
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Objective: The prominent side-effect of cyclosporin A, an immunosuppressive drug, in oral tissues is gingival outgrowth, although the exact mechanism underlying this side-effect is unclear. The main purposes of the present study were to determine whether cyclosporin A induced the gingival outgrowth by promoting proliferation of gingival cells and whether growth factors such as transforming growth factor-βs (TGF-βs), fibroblast growth factor-2 (FGF-2), platelet-derived growth factors (PDGFs), and insulin-like growth factors (IGFs) are involved in the possible changes in the proliferation of gingival cells induced by cyclosporin A.Methods: Cells isolated from rat gingival tissues were cultured with cyclosporin A or IGF-I for 3 days. The effects of cyclosporin A or IGF-I on the proliferation of cultured rat gingival cells were analyzed with a CellTiter 96 proliferation assay kit. The mRNA expression levels for TGF-βs, FGF-2, PDGFs, IGFs, insulin-like growth factor receptors (IGFRs), and insulin-like growth factor binding proteins (IGFBPs) in the rat gingival cells treated with cyclosporin A were measured using competitive reverse transcription–polymerase chain reaction (RT–PCR).Results: Cyclosporin A induced 23–25% (p 〈 0.001) increases in the proliferation of rat gingival cells and approximately 130% (p 〈 0.05) and 60% (p 〈 0.05) elevations in the mRNA expression levels for TGF-β1 and FGF-2, respectively. On the other hand, exogenous IGF-I induced 8–11% (p 〈 0.05) increases in the proliferation, but cyclosporin A induced 30–80% (p 〈 0.05–0.01) reductions in the mRNA expression levels for endogenous IGF-I, IGFR1, IGFBP2, IGFBP3, IGFBP5, and IGFBP6.Conclusions: Cyclosporin A stimulates the proliferation of rat gingival cells. TGF-β1 and FGF-2 could be involved, but IGFs, IGFRs and IGFBPs could not be directly involved in this cyclosporin A induced-stimulation of the gingival cell proliferation.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1600-0765.2004.00762.x
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