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Pesquisa : A14.549.167.900.720.265 [Categoria DeCS]
Referências encontradas : 558 [refinar]
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[PMID]:28665752
[Au] Autor:Wang J; Feng JQ
[Ad] Endereço:1 Biomedical Sciences, Texas A&M College of Dentistry, Dallas, TX, USA.
[Ti] Título:Signaling Pathways Critical for Tooth Root Formation.
[So] Source:J Dent Res;96(11):1221-1228, 2017 Oct.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tooth is made of an enamel-covered crown and a cementum-covered root. Studies on crown dentin formation have been a major focus in tooth development for several decades. Interestingly, the population prevalence for genetic short root anomaly (SRA) with no apparent defects in crown is close to 1.3%. Furthermore, people with SRA itself are predisposed to root resorption during orthodontic treatment. The discovery of the unique role of Nfic (nuclear factor I C; a transcriptional factor) in controlling root but not crown dentin formation points to a new concept: tooth crown and root have different control mechanisms. Further genetic mechanism studies have identified more key molecules (including Osterix, ß-catenin, and sonic hedgehog) that play a critical role in root formation. Extensive studies have also revealed the critical role of Hertwig's epithelial root sheath in tooth root formation. In addition, Wnt10a has recently been found to be linked to multirooted tooth furcation formation. These exciting findings not only fill the critical gaps in our understanding about tooth root formation but will aid future research regarding the identifying factors controlling tooth root size and the generation of a whole "bio-tooth" for therapeutic purposes. This review starts with human SRA and mainly focuses on recent progress on the roles of NFIC-dependent and NFIC-independent signaling pathways in tooth root formation. Finally, this review includes a list of the various Cre transgenic mouse lines used to achieve tooth root formation-related gene deletion or overexpression, as well as strengths and limitations of each line.
[Mh] Termos MeSH primário: Odontogênese/fisiologia
Transdução de Sinais
Raiz Dentária/embriologia
[Mh] Termos MeSH secundário: Animais
Cemento Dentário/embriologia
Dentina/embriologia
Órgão do Esmalte/embriologia
Proteínas Hedgehog/metabolismo
Seres Humanos
Camundongos
Fatores de Transcrição NFI/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Odontogênese/genética
Fator de Transcrição Sp7
Fatores de Transcrição/metabolismo
Proteínas Wnt/metabolismo
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Hedgehog Proteins); 0 (NFI Transcription Factors); 0 (Nerve Tissue Proteins); 0 (Sp7 Transcription Factor); 0 (Sp7 protein, human); 0 (Sp7 protein, mouse); 0 (Transcription Factors); 0 (WNT10A protein, human); 0 (Wnt Proteins); 0 (Wnt10a protein, mouse); 0 (beta Catenin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE
[do] DOI:10.1177/0022034517717478


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[PMID]:27289075
[Au] Autor:Morita T; Fujikawa K; Baba O; Shibata S
[Ad] Endereço:Department of Maxillofacial Anatomy, Division of Maxillofacial and Neck Reconstruction, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
[Ti] Título:An in situ hybridization study of Hyaluronan synthase (Has) mRNA in developing mouse molar and incisor tooth germs.
[So] Source:Gene Expr Patterns;21(1):28-40, 2016 May.
[Is] ISSN:1872-7298
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Hyaluronan (HA) is a major constituent molecule in most extracellular matrices and is synthesized by Hyaluronan synthase (Has). In the present study, we examined expression patterns of Has1, -2, -3 mRNA in developing mouse molar and incisor tooth germs from embryonic day (E) 11.5 to postnatal day (P) 7, focusing on Hertwig's epithelial root sheath (HERS) and the apical bud in particular. Has1 mRNA expression was not detected in all tooth germs examined. Has2 mRNA was expressed in the surrounding mesenchyme from E12.0 to 18.0 in both molar and incisor tooth germs, but disappeared after birth. Meanwhile, Has3 mRNA was exclusively expressed within the enamel organ, especially in the inner enamel epithelium (IEE), stellate reticulum (SR), and stratum intermedium (SI) until the early bell stage at E16.0. Has3 mRNA disappeared as IEE differentiated into differentiating ameloblasts (dABs), but remained in SI until the root developmental stage of the molar tooth germ at P7. Has3 mRNA was also expressed in HERS until P7. In incisors, Has3 mRNA was expressed in the apical bud, especially in the transit-amplifying (TA) cell region from E16.0 to P7, and in the papillary layer (PL) adjacent to the mature enamel. These gene expression patterns suggested that Has3 is the main control factor for prenatal and postnatal HA synthesis of the tooth germ, and may in part regulate crown and root formation of the tooth germ, maintenance of stem cell niches in the apical bud as well as mineral transport in PL.
[Mh] Termos MeSH primário: Desenvolvimento Embrionário/genética
Glucuronosiltransferase/genética
Germe de Dente/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Animais
Órgão do Esmalte/crescimento & desenvolvimento
Órgão do Esmalte/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Glucuronosiltransferase/biossíntese
Hialuronan Sintases
Ácido Hialurônico/metabolismo
Hibridização In Situ
Incisivo/crescimento & desenvolvimento
Incisivo/metabolismo
Mesoderma/crescimento & desenvolvimento
Mesoderma/metabolismo
Camundongos
Dente Molar/crescimento & desenvolvimento
Dente Molar/metabolismo
Odontogênese/genética
RNA Mensageiro/biossíntese
RNA Mensageiro/genética
Germe de Dente/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 9004-61-9 (Hyaluronic Acid); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.212 (Has2 protein, mouse); EC 2.4.1.212 (Has3 protein, mouse); EC 2.4.1.212 (Hyaluronan Synthases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160612
[St] Status:MEDLINE


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[PMID]:26871984
[Au] Autor:Liu B; Han X; Feng W; Cui J; Hasegawa T; Amizuka N; Xu X; Li M
[Ad] Endereço:Department of Bone Metabolism, School of Stomatology, Shandong University, Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Jinan, China; Stomatology Department of Jining Medical University, China.
[Ti] Título:Altered distribution of Ghrelin protein in mice molar development.
[So] Source:Arch Oral Biol;65:82-6, 2016 May.
[Is] ISSN:1879-1506
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Ghrelin, an appetite-stimulating hormone, plays diverse regulatory functions in cell growth, proliferation, differentiation and apoptosis during mammalian development. There is limited information currently available regarding Ghrelin expression during mammalian tooth development, thus we aimed to establish the spatiotemporal expression of Ghrelin during murine molar odontogenesis. DESIGN: Immunohistochemistry was performed to detect the expression pattern of Ghrelin in mandible molar from E15.5 to PN7 during murine tooth development. RESULTS: The results showed that Ghrelin initially expressed in the inner enamel epithelium and the adjacent mesenchymal cells below, further with persistent expression in the ameloblasts and odontoblasts throughout the following developmental stages. In addition, Ghrelin was also present in Hertwig's epithelial root sheath at the beginning of tooth root formation. CONCLUSIONS: These results suggest that Ghrelin was present in tooth organs throughout the stages of tooth development, especially in ameloblasts and odontoblasts with little spatiotemporal expression differences. However, the potential regulatory roles of this hormone in tooth development still need to be validated by functional studies.
[Mh] Termos MeSH primário: Grelina/biossíntese
Grelina/metabolismo
Dente Molar/metabolismo
[Mh] Termos MeSH secundário: Ameloblastos/citologia
Ameloblastos/metabolismo
Animais
Apoptose/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Esmalte Dentário/citologia
Esmalte Dentário/embriologia
Esmalte Dentário/metabolismo
Órgão do Esmalte/embriologia
Órgão do Esmalte/crescimento & desenvolvimento
Órgão do Esmalte/metabolismo
Epitélio/embriologia
Epitélio/metabolismo
Feminino
Imuno-Histoquímica
Camundongos
Camundongos Endogâmicos ICR
Dente Molar/citologia
Dente Molar/efeitos dos fármacos
Dente Molar/crescimento & desenvolvimento
Odontoblastos/citologia
Odontoblastos/metabolismo
Odontogênese/efeitos dos fármacos
Odontogênese/fisiologia
Gravidez
Germe de Dente/embriologia
Germe de Dente/crescimento & desenvolvimento
Germe de Dente/metabolismo
Raiz Dentária/embriologia
Raiz Dentária/crescimento & desenvolvimento
Raiz Dentária/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ghrelin)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170123
[Lr] Data última revisão:
170123
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:160213
[St] Status:MEDLINE


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[PMID]:26763602
[Au] Autor:Papp T; Hollo K; Meszar-Katona E; Nagy Z; Polyak A; Miko E; Bai P; Felszeghy S
[Ad] Endereço:a Department of Anatomy, Histology and Embryology; Faculty of Medicine , University of Debrecen , Debrecen , Hungary ;
[Ti] Título:TLR signalling can modify the mineralization of tooth germ.
[So] Source:Acta Odontol Scand;74(4):307-14, 2016.
[Is] ISSN:1502-3850
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The aim of this work is to investigate the possible role of Toll-like receptor 4 (TLR4) during the development of mouse tooth germ. TLR4 is well known to inhibit mineralization and cause inflammation in mature odontoblasts and dental pulp cells. However, unlike these pathological functions of TLR4, little is known about the developmental function(s) of TLR4 during tooth development. MATERIALS AND METHODS: TLR4 expression was studied via Western blot in developing lower mouse incisors from E13.5 to E18.5. To generate functional data about the effects of TLR4, a specific agonist (LPS) was applied to the medium of in vitro tooth germ cultures, followed by Western blot, histochemical staining, ELISA assay, in situ hybridization and RT-qPCR. RESULTS: Increased accumulation of biotin-labelled LPS was detected in the enamel organ and in preodontoblasts. LPS treatment induced degradation of the inhibitor molecule (IκB) of the NF-κB signalling pathway. However, no morphological alterations were detected in cultured tissue after LPS addition at the applied dosage. Activation of TLR4 inhibited the mineralization of enamel and dentin, as demonstrated by alizarin red staining and as decreased levels of collagen type X. mRNA expression of ameloblastin was elevated after LPS administration. CONCLUSION: These results demonstrate that TLR4 may decrease the mineralization of hard tissues of the tooth germ and may trigger the maturation of ameloblasts; it can give valuable information to understand better congenital tooth abnormalities.
[Mh] Termos MeSH primário: Transdução de Sinais/fisiologia
Receptor 4 Toll-Like/fisiologia
Calcificação de Dente/fisiologia
Germe de Dente/fisiologia
[Mh] Termos MeSH secundário: Ameloblastos/efeitos dos fármacos
Animais
Colágeno Tipo X/análise
Colágeno Tipo X/efeitos dos fármacos
Esmalte Dentário/efeitos dos fármacos
Esmalte Dentário/metabolismo
Proteínas do Esmalte Dentário/análise
Proteínas do Esmalte Dentário/efeitos dos fármacos
Dentina/efeitos dos fármacos
Dentina/metabolismo
Órgão do Esmalte/efeitos dos fármacos
Órgão do Esmalte/metabolismo
Proteínas I-kappa B/análise
Proteínas I-kappa B/efeitos dos fármacos
Lipopolissacarídeos/farmacologia
Camundongos
Odontoblastos/efeitos dos fármacos
Odontoblastos/metabolismo
Odontogênese/efeitos dos fármacos
Odontogênese/fisiologia
Técnicas de Cultura de Órgãos
Transdução de Sinais/efeitos dos fármacos
Receptor 4 Toll-Like/efeitos dos fármacos
Calcificação de Dente/efeitos dos fármacos
Germe de Dente/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ambn protein, mouse); 0 (Collagen Type X); 0 (Dental Enamel Proteins); 0 (I-kappa B Proteins); 0 (IkappaBeta protein, mouse); 0 (Lipopolysaccharides); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:160115
[St] Status:MEDLINE
[do] DOI:10.3109/00016357.2015.1130853


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[PMID]:26715056
[Au] Autor:Le MH; Warotayanont R; Stahl J; Den Besten PK; Nakano Y
[Ad] Endereço:Department of Orofacial Sciences, University of California, San Francisco, School of Dentistry, San Francisco, CA, USA.
[Ti] Título:Amelogenin Exon4 Forms a Novel miRNA That Directs Ameloblast and Osteoblast Differentiation.
[So] Source:J Dent Res;95(4):423-9, 2016 Apr.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Amelogenins constitute the major portion of secretory enamel matrix proteins and are known to be highly alternative spliced. Of all the alternatively spliced forms of amelogenins, exon4 is most commonly spliced out. Our analyses of the exon4 sequence led us to hypothesize that when spliced out, exon4 may generate a novel mature miRNA. To explore this possibility, we used in vivo mouse models (wild-type and Amel knockout mice) and in vitro cell culture to investigate the presence and function of a mature miRNA derived from exon4 (miR-exon4). When ameloblast-like cells (LS8) were transfected with an amelogenin minigene to increase amelogenin synthesis, the transfected cells synthesized miR-exon4. Introduction of a mutation in the conserved CNNC sequence required for primary miRNA recognition, downstream of the mature miR-exon4 sequence, resulted in a significantly reduced production of miR-exon4 in the transfected cells. In vivo, miR-exon4 was most highly amplified from wild-type mouse enamel organs at the secretory stage. In Amel knockout mice, an in vivo model for reduced amelogenin synthesis, we found reduced miR-exon4, with no changes in expression of enamel matrix-related genes. However, expression of Runx2 and its downstream genes Odam and Amtn were significantly downregulated. Transfection of miR-exon4 mimic to the LS8 cells also significantly upregulated Runx2. The mature miR-exon4 as well as Runx2 was also present in mouse osteoblasts with no apparent change in expression level between wild-type and Amel knockout mice. However, transfecting miR-exon4 inhibitor to the MC3T3-E1 osteoblastic cells resulted in a significant downregulation of Runx2 expression. These data indicate that when exon4 is spliced out, as occurs most of the time during alternative splicing of amelogenin pre-mRNA, a novel mature miRNA is generated from exon4. This miR-exon4 may contribute to the differentiation of ameloblasts and osteoblasts through regulation of Runx2 expression.
[Mh] Termos MeSH primário: Ameloblastos/fisiologia
Amelogênese/genética
Amelogenina/metabolismo
Éxons/genética
MicroRNAs/metabolismo
Osteoblastos/fisiologia
Osteogênese/genética
[Mh] Termos MeSH secundário: Animais
Técnicas de Cultura de Células
Diferenciação Celular/fisiologia
Linhagem Celular
Subunidade alfa 1 de Fator de Ligação ao Core/metabolismo
Órgão do Esmalte/metabolismo
Camundongos
Camundongos Knockout
Mutação
Reação em Cadeia da Polimerase
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amelogenin); 0 (Core Binding Factor Alpha 1 Subunit); 0 (MicroRNAs); 0 (Runx2 protein, mouse)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160322
[Lr] Data última revisão:
160322
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:151231
[St] Status:MEDLINE
[do] DOI:10.1177/0022034515622443


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[PMID]:26712243
[Au] Autor:Sóñora C; Arbildi P; Rodríguez-Camejo C; Beovide V; Marco A; Hernández A
[Ad] Endereço:Cátedra de Inmunología, Instituto de Química Biológica, Facultad de Ciencias -Departamento de Biociencias, Facultad de Química, Universidad de la República, Montevideo, Uruguay.
[Ti] Título:Enamel organ proteins as targets for antibodies in celiac disease: implications for oral health.
[So] Source:Eur J Oral Sci;124(1):11-6, 2016 Feb.
[Is] ISSN:1600-0722
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Enamel defects in permanent and deciduous teeth may be oral manifestations of celiac disease. Sometimes they are the only sign that points to this underdiagnosed autoimmune pathology. However, the etiology of these specific enamel defects remains unknown. Based on previously reported cross-reactivity of antibodies to gliadin with the enamel proteins, amelogenin and ameloblastin, we analyzed (using immunohistochemistry) the ability of anti-gliadin IgG, produced during untreated disease, to recognize enamel organ structures. We used swine germ teeth as a tissue model because they are highly homologous to human teeth in terms of proteins and development biology. Strong staining of the enamel matrix and of the layer of ameloblasts was observed with serum samples from women with celiac disease; high IgG reactivity was found against both gliadin peptides and enamel matrix protein extract, but there was no IgG reactivity against tissue antigens. In line with these findings, the gamma globulin fraction from gliadin-immunized BALB/c mice showed a similar staining pattern to that of amelogenin-specific staining. These results strongly suggest a pathological role for antibodies to gliadin in enamel defect dentition for both deciduous and permanent teeth, considering that IgG can be transported through the placenta during fetal tooth development.
[Mh] Termos MeSH primário: Órgão do Esmalte
[Mh] Termos MeSH secundário: Ameloblastos
Amelogenina
Animais
Doença Celíaca
Esmalte Dentário
Proteínas do Esmalte Dentário
Feminino
Seres Humanos
Saúde Bucal
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amelogenin); 0 (Dental Enamel Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:151230
[St] Status:MEDLINE
[do] DOI:10.1111/eos.12241


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[PMID]:26615575
[Au] Autor:Faibish D; Suzuki M; Bartlett JD
[Ad] Endereço:Department of Mineralized Tissue Biology and Harvard School of Dental Medicine, The Forsyth Institute, 245 First Street, Cambridge, MA 02142, USA. Electronic address: dfaibish@forsyth.org.
[Ti] Título:Appropriate real-time PCR reference genes for fluoride treatment studies performed in vitro or in vivo.
[So] Source:Arch Oral Biol;62:33-42, 2016 Feb.
[Is] ISSN:1879-1506
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Quantitative real-time PCR (qPCR) is routinely performed for experiments designed to identify the molecular mechanisms involved in the pathogenesis of dental fluorosis. Expression of reference gene(s) is expected to remain unchanged in fluoride-treated cells or in rodents relative to the corresponding untreated controls. The aim of this study was to select optimal reference genes for fluoride experiments performed in vitro and in vivo. DESIGN: Five candidate genes were evaluated: B2m, Eef1a1, Gapdh, Hprt and Tbp. For in vitro experiments, LS8 cells derived from mouse enamel organ were treated with 0, 1, 3 and/or 5mM sodium fluoride (NaF) for 6 or 18 h followed by RNA isolation. For in vivo experiments, six-week old rats were treated with 0 or 100 ppm fluoride as NaF for six weeks at which time RNA was isolated from enamel organs. RNA from cells and enamel organs were reverse-transcribed and stability of gene expression for the candidate reference genes was evaluated by qPCR in treated versus non-treated samples. RESULTS: The most stably expressed genes in vitro according to geNorm were B2m and Tbp, and according to Normfinder were Hprt and Gapdh. The most stable genes in vivo were Eef1a1 and Gapdh. Expression of Ddit3, a gene previously shown to be induced by fluoride, was demonstrated to be accurately calculated only when using an optimal reference gene. CONCLUSIONS: This study identifies suitable reference genes for relative quantification of gene expression by qPCR after fluoride treatment both in cultured cells and in the rodent enamel organ.
[Mh] Termos MeSH primário: Expressão Gênica/efeitos dos fármacos
Reação em Cadeia da Polimerase em Tempo Real/métodos
Fluoreto de Sódio/farmacologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Órgão do Esmalte/citologia
Órgão do Esmalte/efeitos dos fármacos
Fluorose Dentária/etiologia
Fluorose Dentária/genética
Perfilação da Expressão Gênica
Masculino
Camundongos
Fator 1 de Elongação de Peptídeos/genética
RNA/genética
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real/normas
Padrões de Referência
Fator de Transcrição CHOP/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Ddit3 protein, rat); 0 (EEF1A1 protein, rat); 0 (Peptide Elongation Factor 1); 147336-12-7 (Transcription Factor CHOP); 63231-63-0 (RNA); 8ZYQ1474W7 (Sodium Fluoride)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:151130
[St] Status:MEDLINE


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[PMID]:26613250
[Au] Autor:Lu C; Huguley S; Cui C; Cabaniss LB; Waite PD; Sarver DM; Mamaeva OA; MacDougall M
[Ad] Endereço:Institute of Oral Health Research, School of Dentistry, UAB - The University of Alabama at Birmingham, Birmingham, Ala., USA.
[Ti] Título:Effects of FGFR Signaling on Cell Proliferation and Differentiation of Apert Dental Cells.
[So] Source:Cells Tissues Organs;201(1):26-37, 2016.
[Is] ISSN:1422-6421
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The Apert syndrome is a rare congenital disorder most often arising from S252W or P253R mutations in fibroblast growth factor receptor (FGFR2). Numerous studies have focused on the regulatory role of Apert FGFR2 signaling in bone formation, whereas its functional role in tooth development is largely unknown. To investigate the role of FGFR signaling in cell proliferation and odontogenic differentiation of human dental cells in vitro, we isolated dental pulp and enamel organ epithelia (EOE) tissues from an Apert patient carrying the S252W FGFR2 mutation. Apert primary pulp and EOE cells were established and shown to exhibit normal morphology and express alkaline phosphatase under differentiation conditions. Similar to control cells, Apert dental pulp and EOE cells expressed all FGFRs, with highest levels of FGFR1 followed by FGFR2 and low levels of FGFR3 and FGFR4. However, Apert cells had increased cell growth compared with control cells. Distinct from previous findings in osteoblast cells, gain-of-function S252W FGFR2 mutation did not upregulate the expression of epidermal growth factor receptor (EGFR) and platelet-derived growth factor receptor (PDGFRα), but elevated extracellular signal-regulated kinase (ERK) signaling in cells after EGF stimulation. Unexpectedly, there was little effect of the S252W mutation on odontogenic gene expression in dental pulp and EOE cells. However, after inhibition of total FGFR signaling or ERK signaling, the expression of odontogenic genes was upregulated in both dental cell types, indicating the negative effect of whole FGFR signaling on odontogenic differentiation. This study provides novel insights on FGFR signaling and a common Apert FGFR2 mutation in the regulation of odontogenic differentiation of dental mesenchymal and epithelial cells.
[Mh] Termos MeSH primário: Acrocefalossindactilia/genética
Polpa Dentária/citologia
Órgão do Esmalte/citologia
Odontogênese/genética
Receptor Tipo 2 de Fator de Crescimento de Fibroblastos/genética
Dente/embriologia
[Mh] Termos MeSH secundário: Fosfatase Alcalina/biossíntese
Diferenciação Celular/genética
Proliferação Celular/genética
Células Cultivadas
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Regulação da Expressão Gênica/genética
Seres Humanos
Masculino
Receptor do Fator de Crescimento Epidérmico/biossíntese
Receptor Tipo 1 de Fator de Crescimento de Fibroblastos/biossíntese
Receptor Tipo 2 de Fator de Crescimento de Fibroblastos/biossíntese
Receptor Tipo 3 de Fator de Crescimento de Fibroblastos/biossíntese
Receptor Tipo 4 de Fator de Crescimento de Fibroblastos/biossíntese
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/biossíntese
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (FGFR1 protein, human); EC 2.7.10.1 (FGFR2 protein, human); EC 2.7.10.1 (FGFR3 protein, human); EC 2.7.10.1 (FGFR4 protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 1); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 2); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 3); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 4); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.1.3.1 (Alkaline Phosphatase)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151128
[St] Status:MEDLINE
[do] DOI:10.1159/000441349


  9 / 558 MEDLINE  
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[PMID]:26276269
[Au] Autor:Nel S; van Heerden M; van Heerden W
[Ad] Endereço:Department of Oral Pathology and Oral Biology, School of Dentistry, Faculty of Health Sciences, University of Pretoria, Oral and Dental Hospital, Bophelo Road, Pretoria, South Africa. Electronic address: sulette.nel@up.ac.za.
[Ti] Título:Immunohistochemical expression of CD56 in dog (Canis familiaris) odontogenesis.
[So] Source:Arch Oral Biol;60(10):1577-80, 2015 Oct.
[Is] ISSN:1879-1506
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIM: To investigate the expression of CD56 in dog odontogenesis in order to elucidate the expression found in ameloblastomas. MATERIALS AND METHODS: Immunohistochemical analysis of CD56 expression of developing dog teeth in the bud, cap and bell stages including the remnants of the dental lamina. RESULTS: Weak CD56 expression was observed in the dental epithelium during the bud stage with intense staining of certain peripheral epithelial cells. Positive staining of epithelial cells was also observed in the cap stage with intense staining of the inner enamel epithelium at this stage. During the bell stage the staining was concentrated on the cervical loop areas. The dental papilla revealed positive staining throughout the cap and bell stages while the dental follicle stained intensely positive throughout all the phases examined. The dental lamina and Serres rests also stained positive for CD56. CONCLUSIONS: The expression of CD56 in dog odontogenic tissue varies according to the stage of tooth development. There is a positive correlation between the positive staining observed in ameloblastomas and their odontogenic cells of origin.
[Mh] Termos MeSH primário: Antígeno CD56/biossíntese
Cães/crescimento & desenvolvimento
Cães/metabolismo
Odontogênese/fisiologia
[Mh] Termos MeSH secundário: Ameloblastoma/metabolismo
Ameloblastoma/veterinária
Animais
Diferenciação Celular/fisiologia
Papila Dentária/citologia
Papila Dentária/metabolismo
Órgão do Esmalte/citologia
Órgão do Esmalte/metabolismo
Células Epiteliais/citologia
Células Epiteliais/metabolismo
Feminino
Imuno-Histoquímica/veterinária
Germe de Dente/citologia
Germe de Dente/metabolismo
Nervo Vago/citologia
Nervo Vago/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD56 Antigen)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:150816
[St] Status:MEDLINE


  10 / 558 MEDLINE  
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[PMID]:26276267
[Au] Autor:Kero D; Kalibovic Govorko D; Medvedec Mikic I; Vukojevic K; Cigic L; Saraga-Babic M
[Ad] Endereço:Study Programme of Dental Medicine, School of Medicine, University of Split, Soltanska 2, 21000 Split, Croatia. Electronic address: dkero@mefst.hr.
[Ti] Título:Analysis of expression patterns of IGF-1, caspase-3 and HSP-70 in developing human tooth germs.
[So] Source:Arch Oral Biol;60(10):1533-44, 2015 Oct.
[Is] ISSN:1879-1506
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIMS: To analyze expression patterns of IGF-1, caspase-3 and HSP-70 in human incisor and canine tooth germs during the late bud, cap and bell stages of odontogenesis. MATERIALS AND METHODS: Head areas or parts of jaw containing teeth from 10 human fetuses aged between 9th and 20th developmental weeks were immunohistochemically analyzed using IGF-1, active caspase-3 and HSP-70 markers. Semi-quantitative analysis of each marker's expression pattern was also performed. RESULTS: During the analyzed period, IGF-1 and HSP-70 were mostly expressed in enamel organ. As development progressed, expression of IGF-1 and HSP-70 became more confined to differentiating tissues in the future cusp tip area, as well as in highly proliferating cervical loops. Few apoptotic bodies highly positive to active caspase-3 were observed in enamel organ and dental papilla from the cap stage onward. However, both enamel epithelia moderately expressed active caspase-3 throughout the investigated period. CONCLUSIONS: Expression patterns of IGF-1, active caspase-3 and HSP-70 imply importance of these factors for early human tooth development. IGF-1 and HSP-70 have versatile functions in control of proliferation, differentiation and anti-apoptotic protection of epithelial parts of human enamel organ. Active caspase-3 is partially involved in formation and apoptotic removal of primary enamel knot, although present findings might reflect its ability to perform other non-death functions such as differentiation of hard dental tissues secreting cells and guidance of ingrowth of proliferating cervical loops.
[Mh] Termos MeSH primário: Caspase 3/biossíntese
Proteínas de Choque Térmico HSP70/biossíntese
Fator de Crescimento Insulin-Like I/biossíntese
Germe de Dente/metabolismo
[Mh] Termos MeSH secundário: Diferenciação Celular
Dente Canino/citologia
Dente Canino/embriologia
Dente Canino/metabolismo
Esmalte Dentário/metabolismo
Papila Dentária/citologia
Papila Dentária/embriologia
Papila Dentária/crescimento & desenvolvimento
Papila Dentária/metabolismo
Órgão do Esmalte/citologia
Órgão do Esmalte/embriologia
Órgão do Esmalte/metabolismo
Feto
Seres Humanos
Imuno-Histoquímica
Incisivo/embriologia
Incisivo/metabolismo
Odontogênese
Germe de Dente/citologia
Germe de Dente/embriologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (HSP70 Heat-Shock Proteins); 67763-96-6 (Insulin-Like Growth Factor I); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:150912
[Lr] Data última revisão:
150912
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:150816
[St] Status:MEDLINE



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