Cyclosporin A induces proliferation in human gingival fibroblasts via induction of transforming growth factor-beta 1

dc.creatorCotrim, P
dc.creatorMartelli, H
dc.creatorGraner, E
dc.creatorSauk, JJ
dc.creatorColetta, RD
dc.date2003
dc.dateNOV
dc.date2014-11-18T11:16:22Z
dc.date2015-11-26T17:49:50Z
dc.date2014-11-18T11:16:22Z
dc.date2015-11-26T17:49:50Z
dc.date.accessioned2018-03-29T00:32:57Z
dc.date.available2018-03-29T00:32:57Z
dc.identifierJournal Of Periodontology. Amer Acad Periodontology, v. 74, n. 11, n. 1625, n. 1633, 2003.
dc.identifier0022-3492
dc.identifierWOS:000187316100007
dc.identifier10.1902/jop.2003.74.11.1625
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/57553
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/57553
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/57553
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1289496
dc.descriptionBackground: Cyclosporin A (CsA) is a widely used immunosuppressant that causes significant side effects including gingival overgrowth. The pathogenesis of this condition is not fully understood; however, recent studies show that CsA regulates the transcription of several cytokines including transforming growth factor-beta 1 (TGF-beta1). In this study, we evaluated the effects of CsA and TGF-beta1 on human normal gingival (NG) fibroblast proliferation, and explored a possible autocrine stimulation of TGF-beta1 as a cellular regulator of proliferation induced by CsA in NG fibroblasts. Methods: NG fibroblast cell lines were incubated with increasing concentrations of CsA or TGF-beta1 and the proliferation index determined by automatic cell counting, BrdU incorporation, PCNA expression, and mitotic potential. To determine the effect of TGF-beta1 on the proliferation rate of NG fibroblasts under CsA treatment, NG fibroblast cultures were simultaneously treated with CsA and antisense oligonucleotides against the translation-start site of the TGF-beta1 mRNA. Results: Treatment of NG fibroblasts with CsA or TGF-beta1 significantly stimulated the cell proliferation in a dose-dependent manner. Furthermore, neutralization of TGF-beta1 production in CsA-treated NG fibroblasts inhibited CsA's effect on NG fibroblast proliferation, demonstrating an autocrine stimulatory effect of TGF-beta1 in CsA-treated NG fibroblast proliferation. Conclusion: The results presented here suggest that CsA stimulatory induction of NG fibroblast proliferation is mediated via TGF-beta1 in an autocrine fashion.
dc.description74
dc.description11
dc.description1625
dc.description1633
dc.languageen
dc.publisherAmer Acad Periodontology
dc.publisherChicago
dc.publisherEUA
dc.relationJournal Of Periodontology
dc.relationJ. Periodont.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectCyclosporin A/adverse effects
dc.subjectfibroblasts
dc.subjectgingival
dc.subjectgingival hyperplasia/pathogenesis
dc.subjectgrowth factors
dc.subjecttransforming
dc.subjectGrowth-factor-beta
dc.subjectPeriodontal-ligament Cells
dc.subjectMatrix Metalloproteinases
dc.subjectAutocrine Stimulation
dc.subjectAllograft Recipients
dc.subjectTgf-beta-1
dc.subjectExpression
dc.subjectOvergrowth
dc.subjectHeterogeneity
dc.subjectPathogenesis
dc.titleCyclosporin A induces proliferation in human gingival fibroblasts via induction of transforming growth factor-beta 1
dc.typeArtículos de revistas


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