Transforming growth factor-beta 1 autocrine stimulation regulates fibroblast proliferation in hereditary gingival fibromatosis

dc.creatorde Andrade, CR
dc.creatorCotrin, P
dc.creatorGraner, E
dc.creatorAlmeida, OP
dc.creatorSauk, JJ
dc.creatorColetta, RD
dc.date2001
dc.dateDEC
dc.date2014-11-15T22:16:28Z
dc.date2015-11-26T17:22:18Z
dc.date2014-11-15T22:16:28Z
dc.date2015-11-26T17:22:18Z
dc.date.accessioned2018-03-29T00:09:46Z
dc.date.available2018-03-29T00:09:46Z
dc.identifierJournal Of Periodontology. Amer Acad Periodontology, v. 72, n. 12, n. 1726, n. 1733, 2001.
dc.identifier0022-3492
dc.identifierWOS:000173250600012
dc.identifier10.1902/jop.2001.72.12.1726
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/77550
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/77550
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/77550
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1283575
dc.descriptionBackground: Hereditary gingival fibromatosis (HGF) is a rare oral disease characterized by a slow and progressive enlargement of both the maxilla and mandible gingiva. Increased proliferation, elevated synthesis of extracellular matrix, particularly Collagen, and reduced levels of matrix metalloproteinases seem to contribute to the pathogenesis of gingival overgrowth in HGF patients. Transforming growth factor-beta1 (TGF-beta1) is an important cytokine thought to play a major role in fibrotic disorders such as HGF due to its ability to stimulate the synthesis and reduce the degradation of extracellular matrix. In HGF fibroblasts, TGF-beta1 autocrine stimulation reduces expression and production of matrix metalloproteinases. However, the role of TGF-beta1 in fibroblast growth modulation has not been established in this disease. Methods: The aim of this study was to confirm the increased proliferation rate of HGF fibroblast cell lines and to explore a possible autocrine role of TGF-beta1 as a cell growth stimulator by blocking production of this endogenous cytokine using 2 well-established systems: antisense oligonucleotides and neutralizing antibodies. Results: Four different cellular proliferation assays, bromodeoxyuridine labeling, argyrophilic nucleolar organizing region staining, proliferating cell nuclear antigen, and mitotic indexes, confirmed that fibroblasts from HGF proliferate significantly faster than those from normal gingiva. Antisense oligonucleotides reduced TGF-beta1 production as demonstrated by capture enzyme-linked immunosorbent assay, whereas TGF-beta1 expression levels were not significantly modified. Blocking TGF-beta1 synthesis with oligonucleotides or its activity with specific antibodies resulted in a decreased magnitude of HGF fibroblast proliferation. Conclusion: These results are consistent with the existence of an autocrine role of TGF-beta1 as a stimulator of HGF fibroblast proliferation.
dc.description72
dc.description12
dc.description1726
dc.description1733
dc.languageen
dc.publisherAmer Acad Periodontology
dc.publisherChicago
dc.publisherEUA
dc.relationJournal Of Periodontology
dc.relationJ. Periodont.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectfibroblasts, gingival
dc.subjectfibromatosis, gingival
dc.subjectgrowth factors, transforming
dc.subjectproliferation index
dc.subjectFactor-beta
dc.subjectTgf-beta-1
dc.subjectHyperplasia
dc.subjectExpression
dc.subjectCells
dc.subject2p21
dc.titleTransforming growth factor-beta 1 autocrine stimulation regulates fibroblast proliferation in hereditary gingival fibromatosis
dc.typeArtículos de revistas


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