title: Expression of transforming growth factor-beta receptor II mRNA in cyclosporine-induced gingival overgrowth.
abstract: Gingival overgrowth (GO), characterized by increased cellular and extracellular matrix components in gingival tissue, is a frequent side effect of cyclosporine (CsA). In previous studies, elevated levels of transforming growth factor-beta (TGF-beta) have been detected in GO tissue, which led to the conclusion that TGF-beta plays a major part in the pathogenesis. TGF-beta activity is mediated by three receptors; TGF-beta receptor II (TGF-beta RII), the most important, has been immunohistochemically detected in GO and normal gingival tissue. The aim of this study was to clarify whether TGF-beta RII is overexpressed in CsA-induced GO. The expression of TGF-beta RII mRNA in GO tissue of patients on CsA (n = 10, 5 women, aged 42.5 +/- 14.9 years) with renal transplantation (transplant duration 3.6 +/- 0.96 years) was compared with that in healthy gingiva of control subjects (n = 10, 5 women, aged 42.5 +/- 7.6 years). Semiquantitative reverse transcribed-polymerase chain reactions (RT-PCR) were applied with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as an internal standard. TGF-beta RII mRNA was readily detected in the GO tissue of patients on CsA. The level of TGF-beta RII mRNA relative to GAPDH in GO cases was not significantly higher than the relative TGF-beta mRNA level in normal gingiva (0.60 +/- 0.16 vs 0.52 +/- 0.19; P = .575). The precise mechanism of CsA-induced GO remains uncertain. According to our results, TGF-beta RII was not upregulated in CsA-induced GO, and may have no important role in this disorder. However, the involvement of TGF-beta in the molecular pathology of GO may be mediated via TGF-beta RI or RIII.
authors.affiliation: Department of Periodontology, Eastman Dental Institute, University College London, London, UK.
authors.forename: V
authors.initials: V
authors.lastname: Stefanidou
authors.forename: V
authors.initials: V
authors.lastname: Liakopoulos
authors.forename: T
authors.initials: T
authors.lastname: Eleftheriadis
authors.forename: G
authors.initials: G
authors.lastname: Anifandis
authors.forename: P R
authors.initials: PR
authors.lastname: Mertens
authors.forename: E
authors.initials: E
authors.lastname: Kanelaki
authors.forename: I
authors.initials: I
authors.lastname: Stefanidis
mesh_terms: D000328:Adult; D001483:Base Sequence; D003442:Crowns; D016572:Cyclosporine / Q000009:adverse effects*; D017931:DNA Primers; D018076:DNA, Complementary / Q000235:genetics; D005260:Female; D005881:Gingiva / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D007166:Immunosuppressive Agents / Q000009:adverse effects; D016030:Kidney Transplantation / Q000276:immunology; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D017346:Protein Serine-Threonine Kinases; D012333:RNA, Messenger / Q000235:genetics; D000077294:Receptor, Transforming Growth Factor-beta Type II; D018125:Receptors, Transforming Growth Factor beta / Q000235:genetics*; D012016:Reference Values
chemical_list: D017931:DNA Primers; D018076:DNA, Complementary; D007166:Immunosuppressive Agents; D012333:RNA, Messenger; D018125:Receptors, Transforming Growth Factor beta; D016572:Cyclosporine; D017346:Protein Serine-Threonine Kinases; D000077294:Receptor, Transforming Growth Factor-beta Type II