dc.creatorSilvério, K G
dc.creatorDavidson, K C
dc.creatorJames, R G
dc.creatorAdams, A M
dc.creatorFoster, B L
dc.creatorNociti, F H
dc.creatorSomerman, M J
dc.creatorMoon, R T
dc.date2012-Jun
dc.date2015-11-27T13:29:15Z
dc.date2015-11-27T13:29:15Z
dc.date.accessioned2018-03-29T01:16:50Z
dc.date.available2018-03-29T01:16:50Z
dc.identifierJournal Of Periodontal Research. v. 47, n. 3, p. 309-19, 2012-Jun.
dc.identifier1600-0765
dc.identifier10.1111/j.1600-0765.2011.01433.x
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/22150562
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/200390
dc.identifier22150562
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1300623
dc.descriptionBone morphogenetic protein 2 (BMP2)-induced osteogenic differentiation has been shown to occur through the canonical Wnt/βcatenin pathway, whereas factors promoting canonical Wnt signaling in cementoblasts inhibit cell differentiation and promote cell proliferation in vitro. The aim of this study was to investigate whether putative precursor cells of cementoblasts, dental follicle cells (murine SVF4 cells), when stimulated with BMP2, would exhibit changes in genes/proteins associated with the Wnt/β-catenin pathway. SVF4 cells were stimulated with BMP2, and the following assays were carried out: (i) Wnt/β-catenin pathway activation assessed by western blotting, β-catenin/transcription factor (TCF) reporter assays and expression of the lymphoid enhancer-binding factor-1 (Lef1), transcription factor 7 (Tcf7), Wnt inhibitor factor 1 (Wif1) and Axin2 (Axin2) genes; and (ii) cementoblast/osteoblast differentiation assessed by mineralization in vitro, and by the mRNA levels of runt-related transcription factor 2 (Runx2), osterix (Osx), alkaline phosphatase (Alp), osteocalcin (Ocn) and bone sialoprotein (Bsp), determined by quantitative PCR after treatment with wingless-type MMTV integration site family, member 3A (WNT3A) and knockdown of β-catenin. WNT3A induced β-catenin nuclear translocation and up-regulated the transcriptional activity of a canonical Wnt-responsive reporter, suggesting that the Wnt/β-catenin pathway functions in SVF4 cells. Activation of Wnt signaling with WNT3A suppressed BMP2-mediated induction of cementoblast/osteoblast maturation of SVF4 cells. However, β-catenin knockdown showed that the BMP2-induced expression of cementoblast/osteoblast differentiation markers requires endogenous β-catenin. WNT3A down-regulated transcripts for Runx2, Alp and Ocn in SVF4 cells compared with untreated cells. In contrast, BMP2 induction of Bsp transcripts occurred independently of Wnt/β-catenin signaling. These data suggest that stabilization of β-catenin by WNT3A inhibits BMP2-mediated induction of cementoblast/osteoblast differentiation in SVF4 cells, although BMP2 requires endogenous Wnt/β-catenin signaling to promote cell maturation.
dc.description47
dc.description309-19
dc.languageeng
dc.relationJournal Of Periodontal Research
dc.relationJ. Periodont. Res.
dc.rightsfechado
dc.rights© 2011 John Wiley & Sons A/S.
dc.sourcePubMed
dc.subjectAlkaline Phosphatase
dc.subjectAnimals
dc.subjectAxin Protein
dc.subjectBone Morphogenetic Protein 2
dc.subjectCell Culture Techniques
dc.subjectCell Differentiation
dc.subjectCell Line
dc.subjectCell Proliferation
dc.subjectCore Binding Factor Alpha 1 Subunit
dc.subjectDental Cementum
dc.subjectDental Sac
dc.subjectExtracellular Matrix Proteins
dc.subjectGene Knockdown Techniques
dc.subjectHepatocyte Nuclear Factor 1-alpha
dc.subjectIntercellular Signaling Peptides And Proteins
dc.subjectLymphoid Enhancer-binding Factor 1
dc.subjectMice
dc.subjectOsteoblasts
dc.subjectOsteocalcin
dc.subjectOsteogenesis
dc.subjectOsteopontin
dc.subjectT Cell Transcription Factor 1
dc.subjectTranscription Factors
dc.subjectTranscription, Genetic
dc.subjectWnt Signaling Pathway
dc.subjectWnt3a Protein
dc.subjectZinc Fingers
dc.subjectBeta Catenin
dc.titleWnt/β-catenin Pathway Regulates Bone Morphogenetic Protein (bmp2)-mediated Differentiation Of Dental Follicle Cells.
dc.typeArtículos de revistas


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