Base de dados : MEDLINE
Pesquisa : A11.329.522 [Categoria DeCS]
Referências encontradas : 2662 [refinar]
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  1 / 2662 MEDLINE  
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[PMID]:29267673
[Au] Autor:Yan Y; Qi S; Gong SQ; Shang G; Zhao Y
[Ad] Endereço:Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Department of Pediatric Dentistry, Shanghai, China.
[Ti] Título:Effect of CRABP2 on the proliferation and odontoblastic differentiation of hDPSCs.
[So] Source:Braz Oral Res;31:e112, 2017 Dec 18.
[Is] ISSN:1807-3107
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Cellular retinoic acid-binding protein 2 (CRABP2) has been detected in several organs during embryonic development. Recent studies have demonstrated that CRABP2 plays important roles in the retinoic acid, ß-catenin and Notch signaling pathways, as well as in the interaction between epithelial and mesenchymal cells, which are important for human dental pulp stem cells (hDPSCs) and tooth development. In the present study, the expression of CRABP2 during mouse molar development and the role of CRABP2 in hDPSC odontoblastic differentiation were evaluated. CRABP2 was gradually decreased during the development of the first maxillary molar, which exhibited the same trend as the expression of CRABP2 during the odontoblastic induction of hDPSCs. CRABP2 knockdown inhibited the proliferative ability of hDPSCs, while it enhanced odontoblastic differentiation via promoting mineralization nodule formation and upregulating the activity of alkaline phosphatase and the expression of mineralization-related genes. The present study uncovered a novel function of CRABP2 in hDPSCs. Our data suggest that CRABP2 may act as a regulator during the proliferation and differentiation of hDPSCs.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Proliferação Celular/fisiologia
Polpa Dentária/citologia
Odontoblastos/fisiologia
Receptores do Ácido Retinoico/fisiologia
Células-Tronco/fisiologia
[Mh] Termos MeSH secundário: Fosfatase Alcalina
Análise de Variância
Animais
Antraquinonas
Western Blotting
Comunicação Celular
Células Cultivadas
Corantes
Regulação para Baixo/fisiologia
Feminino
Seres Humanos
Imuno-Histoquímica
Masculino
Camundongos Endogâmicos C57BL
Receptores do Ácido Retinoico/análise
Valores de Referência
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthraquinones); 0 (Coloring Agents); 0 (Receptors, Retinoic Acid); 0 (retinoic acid binding protein II, cellular); 60MEW57T9G (alizarin); EC 3.1.3.1 (Alkaline Phosphatase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


  2 / 2662 MEDLINE  
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Costa, Carlos Alberto de Souza
Texto completo SciELO Brasil
[PMID]:29267665
[Au] Autor:Leite MLAES; Soares DG; Basso FG; Hebling J; Costa CAS
[Ad] Endereço:Universidade Estadual Paulista "Júlio de Mesquita Filho" - Unesp, School of Dentistry, Department of Dental Materials and Prosthodontics, Araraquara, SP, Brazil.
[Ti] Título:Biostimulatory effects of simvastatin on MDPC-23 odontoblast-like cells.
[So] Source:Braz Oral Res;31:e104, 2017 Dec 18.
[Is] ISSN:1807-3107
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to evaluate the bioactivity and cytocompatibility of simvastatin (SV) applied to MDPC-23 odontoblast-like cells. For this purpose, MDPC-23 cells were seeded in 96-well plates and submitted to treatments with 0.01 or 0.1 µM of SV for 24 h, 72 h or continuously throughout the experimental protocol. The negative control group (NC) was maintained in DMEM. Cell viability (MTT), ALP activity (thymolphthalein monophosphate), and mineralized matrix deposition (alizarin red) were analyzed at several time points. The data were submitted to ANOVA and Tukey's test (α = 0.05). Although cell viability was observed in the groups treated with SV, these groups did not differ from the NC up to 7 days. There was a reduction in cell viability for the groups treated with 0.1 µM of SV for 72 h, and submitted to continuous mode after 14 days. A significant increase in ALP activity occurred in the group treated with 0.01 µM of SV for 24 h, compared with the NC; however, only the group treated with 0.1 µM of SV in continuous mode reduced the ALP activity, in comparison with the NC. After 14 days, only continuous treatment with 0.1 µM of SV did not differ from NC, whereas the other experimental groups showed increased mineralized matrix deposition. Thus, it was concluded that low concentrations of simvastatin were bioactive and cytocompatible when applied for short periods to cultured MDPC-23 odontoblast-like cells.
[Mh] Termos MeSH primário: Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia
Odontoblastos/efeitos dos fármacos
Sinvastatina/farmacologia
[Mh] Termos MeSH secundário: Animais
Antraquinonas
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Ratos
Valores de Referência
Timolftaleína/análogos & derivados
Timolftaleína/análise
Fatores de Tempo
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthraquinones); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 17016-43-2 (thymolphthalein monophosphate); 60MEW57T9G (alizarin); AGG2FN16EV (Simvastatin); YG5I28WSQP (Thymolphthalein)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


  3 / 2662 MEDLINE  
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[PMID]:29223396
[Au] Autor:Matsuishi YI; Kato H; Masuda K; Yamaza H; Hirofuji Y; Sato H; Wada H; Kiyoshima T; Nonaka K
[Ad] Endereço:Section of Oral Medicine for Children, Division of Oral Health, Growth and Development, Faculty of Dental Science, Kyushu University, 3-1-1 Maidashi, Higashi-Ku, Fukuoka 812-8582, Japan.
[Ti] Título:Accelerated dentinogenesis by inhibiting the mitochondrial fission factor, dynamin related protein 1.
[So] Source:Biochem Biophys Res Commun;495(2):1655-1660, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Undifferentiated odontogenic epithelium and dental papilla cells differentiate into ameloblasts and odontoblasts, respectively, both of which are essential for tooth development. These differentiation processes involve dramatic functional and morphological changes of the cells. For these changes to occur, activation of mitochondrial functions, including ATP production, is extremely important. In addition, these changes are closely related to mitochondrial fission and fusion, known as mitochondrial dynamics. However, few studies have focused on the role of mitochondrial dynamics in tooth development. The purpose of this study was to clarify this role. We used mouse tooth germ organ cultures and a mouse dental papilla cell line with the ability to differentiate into odontoblasts, in combination with knockdown of the mitochondrial fission factor, dynamin related protein (DRP)1. In organ cultures of the mouse first molar, tooth germ developed to the early bell stage. The amount of dentin formed under DRP1 inhibition was significantly larger than that of the control. In experiments using a mouse dental papilla cell line, differentiation into odontoblasts was enhanced by inhibiting DRP1. This was associated with increased mitochondrial elongation and ATP production compared to the control. These results suggest that DRP1 inhibition accelerates dentin formation through mitochondrial elongation and activation. This raises the possibility that DRP1 might be a therapeutic target for developmental disorders of teeth.
[Mh] Termos MeSH primário: Dentinogênese/fisiologia
Dinaminas/antagonistas & inibidores
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/biossíntese
Ameloblastos/citologia
Ameloblastos/fisiologia
Animais
Diferenciação Celular/genética
Diferenciação Celular/fisiologia
Linhagem Celular
Dinaminas/genética
Dinaminas/fisiologia
Proteínas da Matriz Extracelular/biossíntese
Feminino
Camundongos
Camundongos Endogâmicos C57BL
Dinâmica Mitocondrial/fisiologia
Odontoblastos/citologia
Odontoblastos/fisiologia
Técnicas de Cultura de Órgãos
Fosfoproteínas/biossíntese
Gravidez
RNA Interferente Pequeno/genética
Sialoglicoproteínas/biossíntese
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 (Extracellular Matrix Proteins); 0 (Phosphoproteins); 0 (RNA, Small Interfering); 0 (Sialoglycoproteins); 0 (dentin sialophosphoprotein); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.5.5 (Dnm1l protein, mouse); EC 3.6.5.5 (Dynamins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171211
[St] Status:MEDLINE


  4 / 2662 MEDLINE  
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[PMID]:28926618
[Au] Autor:Torres-da-Silva KR; Tessarin GWL; Dias CA; Guiati IZ; Ervolino E; Gonçalves A; Beneti IM; Lovejoy DA; Casatti CA
[Ad] Endereço:Institute of Biosciences of Botucatu, São Paulo State University, Botucatu, São Paulo, Brazil.
[Ti] Título:Teneurin-2 presence in rat and human odontoblasts.
[So] Source:PLoS One;12(9):e0184794, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Teneurins are transmembrane proteins consisting of four paralogues (Ten-1-4), notably expressed in the central nervous system during development. All teneurins contain a bioactive peptide in their carboxyl terminal named teneurin C-terminal associated peptide (TCAP). The present study analyzed the detailed distribution of teneurin-2-like immunoreactive (Ten-2-LI) cells in developing and mature rat molar teeth, as well as in mature human dental pulps. Ten-2 and TCAP-2 genic expressions were also evaluated in rat and human dental pulps. Finally, Ten-2-LI cells were analyzed during the repair process after dentin-pulp complex injury in rat lower molar teeth. For this, histological sections of rat molar teeth and human dental pulps were submitted to immunohistochemical techniques, while total RNA from developing rat teeth and mature human dental pulps were submitted to conventional RT-PCR. Ten-2-LI cells were evident in the initial bell stage of rat molar teeth development, especially in ectomesenchymal cells of the dental papilla. Ten-2-LI odontoblasts showed strong immunoreactivity in rat and human mature teeth. Ten-2 and TCAP-2 genic expressions were confirmed in rat and human dental pulps. Dentin-pulp complex injury resulted in a decrease of Ten-2-LI odontoblasts after traumatic injury. Interestingly, Ten-2-LI cells were also evident in the pulp cell-rich zone in all postoperative days. In conclusion, Ten-2-LI presence in rat and human odontoblasts was demonstrated for the first time and Ten-2/TCAP-2 genic expressions were confirmed in rat and human dental pulps. Furthermore, it was revealed that Ten-2-LI rat odontoblasts can be modulated during the regenerative process.
[Mh] Termos MeSH primário: Proteínas do Tecido Nervoso/metabolismo
Odontoblastos/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Polpa Dentária/citologia
Polpa Dentária/metabolismo
Polpa Dentária/patologia
Dentina/metabolismo
Dentina/patologia
Feminino
Seres Humanos
Imuno-Histoquímica
Masculino
Microscopia Confocal
Dente Molar/crescimento & desenvolvimento
Dente Molar/metabolismo
Dente Molar/patologia
Dente Serotino/citologia
Dente Serotino/metabolismo
Dente Serotino/patologia
Proteínas do Tecido Nervoso/genética
Odontoblastos/citologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nerve Tissue Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184794


  5 / 2662 MEDLINE  
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[PMID]:28678949
[Au] Autor:Tang J; Saito T
[Ad] Endereço:Health Sciences University of Hokkaido, School of Dentistry, Department of Oral Rehabilitation, Division of Clinical Cariology and Endodontology, Hokkaido, Japan.
[Ti] Título:Human plasma fibronectin promotes proliferation and differentiation of odontoblast.
[So] Source:J Appl Oral Sci;25(3):299-309, 2017 May-Jun.
[Is] ISSN:1678-7765
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Objective: To assess the effect of fibronectin (Fn) and porcine type I collagen (PCOL) on odontoblast-like cells in vitro. Material and Methods: Rat odontoblast-like cells (MDPC-23 cells) were inoculated and cultured on Fn-coated or type I collagen-coated substrates. Proliferation assay, alkaline phosphatase activity (ALP activity), mRNA expression of hard tissue-forming markers, and Alizarin red staining were investigated over a period of 10 days. Results: Cells maintained a high proliferation activity on Fn and PCOL even at a low seeding concentration (0.5×104/mL) as demonstrated by CCK-8 assay. The proliferation activity of cells on Fn increases in a concentration-dependent manner while it reached a plateau after 10 µg/mL. Cells adopted long, thin and spindle shape on Fn(10-50) and PCOL. Parallel actin filaments were observed in MDPC-23 cells cultured on Fn and PCOL. ALP activity was markedly up-regulated on Fn and PCOL-coated surfaces. Importantly, gene expression of BSP (Fn10: 2.44±0.32; Fn20: 3.05±0.01; Fn30: 2.90±0.21; Fn40: 2.74±0.30; Fn50: 2.64±0.12; PCOL: 2.20±0.03) and OCN (Fn10: 2.52±0.23; Fn20: 2.28±0.24; Fn30: 2.34±0.21; Fn40: 2.34±0.25; Fn50: 2.20±0.22; PCOL: 1.56±0.16) was significantly enhanced on Fn and PCOL substrates as compared with control; moreover, expression of integrin beta 1 (ITGB1), an ubiquitous cell surface receptor was augmented in Fn(10-50) and PCOL groups simultaneously. In accordance with the ALP activity and gene expression data, calcific deposition in cells grown on Fn(10-50) and PCOL was observed as well. Conclusion: Despite the limitation of this study, the findings indicate that a surface coating of Fn enhances the proliferation, differentiation and mineralization of odontoblast-like cells by activation of integrin beta 1 (ITG B1). The promoting effects of Fn on MDPC-23 cells were achieved at a comparatively lower coating concentration than type I collagen (300 µg/mL). Specifically, it is suggested that the optimum coating concentration of Fn to be 10 µg/mL.
[Mh] Termos MeSH primário: Diferenciação Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Fibronectinas/farmacologia
Odontoblastos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Fosfatase Alcalina/análise
Animais
Antraquinonas
Células Cultivadas
Colágeno Tipo I/farmacologia
Imunofluorescência
Expressão Gênica
Seres Humanos
Integrina beta1/farmacologia
Ratos
Reprodutibilidade dos Testes
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthraquinones); 0 (Collagen Type I); 0 (Fibronectins); 0 (Integrin beta1); 60MEW57T9G (alizarin); EC 3.1.3.1 (Alkaline Phosphatase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170706
[St] Status:MEDLINE


  6 / 2662 MEDLINE  
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[PMID]:28576771
[Au] Autor:Feng J; Jing J; Li J; Zhao H; Punj V; Zhang T; Xu J; Chai Y
[Ad] Endereço:Center for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA 90033, USA.
[Ti] Título:BMP signaling orchestrates a transcriptional network to control the fate of mesenchymal stem cells in mice.
[So] Source:Development;144(14):2560-2569, 2017 07 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Signaling pathways are used reiteratively in different developmental processes yet produce distinct cell fates through specific downstream transcription factors. In this study, we used tooth root development as a model with which to investigate how the BMP signaling pathway regulates transcriptional complexes to direct the fate determination of multipotent mesenchymal stem cells (MSCs). We first identified the MSC population supporting mouse molar root growth as Gli1 cells. Using a Gli1-driven Cre-mediated recombination system, our results provide the first evidence that BMP signaling activity is required for the odontogenic differentiation of MSCs. Specifically, we identified the transcription factors Pax9, Klf4, Satb2 and Lhx8 as being downstream of BMP signaling and expressed in a spatially restricted pattern that is potentially involved in determining distinct cellular identities within the dental mesenchyme. Finally, we found that overactivation of one key transcription factor, Klf4, which is associated with the odontogenic region, promotes odontogenic differentiation of MSCs. Collectively, our results demonstrate the functional significance of BMP signaling in regulating MSC fate during root development and shed light on how BMP signaling can achieve functional specificity in regulating diverse organ development.
[Mh] Termos MeSH primário: Proteínas Morfogenéticas Ósseas/metabolismo
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas Morfogenéticas Ósseas/genética
Diferenciação Celular/genética
Diferenciação Celular/fisiologia
Linhagem da Célula/genética
Linhagem da Célula/fisiologia
Feminino
Redes Reguladoras de Genes
Masculino
Camundongos
Camundongos Transgênicos
Odontoblastos/citologia
Odontoblastos/metabolismo
Odontogênese/genética
Odontogênese/fisiologia
Regeneração/genética
Regeneração/fisiologia
Transdução de Sinais/genética
Transdução de Sinais/fisiologia
Nicho de Células-Tronco/genética
Nicho de Células-Tronco/fisiologia
Raiz Dentária/citologia
Raiz Dentária/crescimento & desenvolvimento
Raiz Dentária/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Proteína GLI1 em Dedos de Zinco/genética
Proteína GLI1 em Dedos de Zinco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Gli protein, mouse); 0 (Transcription Factors); 0 (Zinc Finger Protein GLI1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170604
[St] Status:MEDLINE
[do] DOI:10.1242/dev.150136


  7 / 2662 MEDLINE  
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[PMID]:28494020
[Au] Autor:Iwamoto T; Nakamura T; Ishikawa M; Yoshizaki K; Sugimoto A; Ida-Yonemochi H; Ohshima H; Saito M; Yamada Y; Fukumoto S
[Ad] Endereço:Department of Pediatric Dentistry, Institute of Biomedical Sciences, Tokushima University Graduate School, Kuramoto-cho, Tokushima, Japan.
[Ti] Título:Pannexin 3 regulates proliferation and differentiation of odontoblasts via its hemichannel activities.
[So] Source:PLoS One;12(5):e0177557, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Highly coordinated regulation of cell proliferation and differentiation contributes to the formation of functionally shaped and sized teeth; however, the mechanism underlying the switch from cell cycle exit to cell differentiation during odontogenesis is poorly understood. Recently, we identified pannexin 3 (Panx3) as a member of the pannexin gap junction protein family from tooth germs. The expression of Panx3 was predominately localized in preodontoblasts that arise from dental papilla cells and can differentiate into dentin-secreting odontoblasts. Panx3 also co-localized with p21, a cyclin-dependent kinase inhibitor protein, in preodontoblasts. Panx3 was expressed in primary dental mesenchymal cells and in the mDP dental mesenchymal cell line. Both Panx3 and p21 were induced during the differentiation of mDP cells. Overexpression of Panx3 in mDP cells reduced cell proliferation via up-regulation of p21, but not of p27, and promoted the Bone morphogenetic protein 2 (BMP2)-induced phosphorylation of Smad1/5/8 and the expression of dentin sialophosphoprotein (Dspp), a marker of differentiated odontoblasts. Furthermore, Panx3 released intracellular ATP into the extracellular space through its hemichannel and induced the phosphorylation of AMP-activated protein kinase (AMPK). 5-Aminoimidazole-4-carboxamide-ribonucleoside (AICAR), an activator of AMPK, reduced mDP cell proliferation and induced p21 expression. Conversely, knockdown of endogenous Panx3 by siRNA inhibited AMPK phosphorylation, p21 expression, and the phosphorylation of Smad1/5/8 even in the presence of BMP2. Taken together, our results suggest that Panx3 modulates intracellular ATP levels, resulting in the inhibition of odontoblast proliferation through the AMPK/p21 signaling pathway and promotion of cell differentiation by the BMP/Smad signaling pathway.
[Mh] Termos MeSH primário: Diferenciação Celular
Conexinas/metabolismo
Odontoblastos/citologia
Odontoblastos/metabolismo
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/metabolismo
Trifosfato de Adenosina/metabolismo
Aminoimidazol Carboxamida/análogos & derivados
Aminoimidazol Carboxamida/farmacologia
Animais
Proteínas Morfogenéticas Ósseas/metabolismo
Diferenciação Celular/efeitos dos fármacos
Diferenciação Celular/genética
Proliferação Celular/efeitos dos fármacos
Conexinas/genética
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Papila Dentária/citologia
Ativação Enzimática/efeitos dos fármacos
Proteínas da Matriz Extracelular/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Espaço Intracelular/metabolismo
Camundongos Endogâmicos ICR
Modelos Biológicos
Odontoblastos/efeitos dos fármacos
Fosfoproteínas/metabolismo
Fosforilação/efeitos dos fármacos
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Interferente Pequeno/metabolismo
Ribonucleotídeos/farmacologia
Sialoglicoproteínas/metabolismo
Transdução de Sinais/efeitos dos fármacos
Proteínas Smad/metabolismo
Germe de Dente/metabolismo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Connexins); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (Extracellular Matrix Proteins); 0 (Phosphoproteins); 0 (RNA, Messenger); 0 (RNA, Small Interfering); 0 (Ribonucleotides); 0 (Sialoglycoproteins); 0 (Smad Proteins); 0 (dentin sialophosphoprotein); 0 (pannexin 3 protein, mouse); 360-97-4 (Aminoimidazole Carboxamide); 8L70Q75FXE (Adenosine Triphosphate); EC 2.7.11.31 (AMP-Activated Protein Kinases); F0X88YW0YK (AICA ribonucleotide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177557


  8 / 2662 MEDLINE  
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[PMID]:28489485
[Au] Autor:Matsumura S; Quispe-Salcedo A; Schiller CM; Shin JS; Locke BM; Yakar S; Shimizu E
[Ad] Endereço:1 Department of Oral and Maxillofacial Radiology, University of Connecticut Health Center, School of Dental Medicine, Farmington, Connecticut, USA.
[Ti] Título:IGF-1 Mediates EphrinB1 Activation in Regulating Tertiary Dentin Formation.
[So] Source:J Dent Res;96(10):1153-1161, 2017 Sep.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Eph receptors belong to a subfamily of receptor tyrosine kinases that are activated by membrane-spanning ligands called ephrins. Previously, we demonstrated that the ephrinB1-EphB2 interaction regulates odontogenic/osteogenic differentiation from dental pulp cells (DPCs) in vitro. The goal of this study was to identify the molecular mechanisms regulated by the EphB2/ephrinB1 system that govern tertiary dentin formation in vitro and in vivo. During tooth development, ephrinB1, and EphB2 were expressed in preodontoblast and odontoblasts at postnatal day 4. EphrinB1 was continuously expressed in odontoblasts and odontoblastic processes until the completion of tooth eruption. In addition, ephrinB1 was expressed in odontoblastic processes 2 wk following tooth injury without pulp exposure, whereas EphB2 was expressed in the center of pulp niches but not odontoblasts. In a model of tooth injury with pulp exposure, ephrinB1 was strongly expressed in odontoblasts 4 wk postinjury. In vitro studies with human and mouse DPCs treated with calcium hydroxide (CH) or mineral trioxide aggregate (MTA) showed an increased expression of insulin-like growth factor 1 (IGF-1). Experiments using several inhibitors of IGF-1 receptor signaling revealed that inhibiting the Ras/Raf-1/MAPK pathway inhibited EphB2 expression, and inhibiting the PI3K/Akt/mTOR pathway specifically inhibited ephrinB1 gene expression. Tooth injury in mice with odontoblast-specific IGF-1 receptor ablation exhibited a reduced tertiary dentin volume, mineral density, and ephrinB1 expression 4 wk following injury. We conclude that the IGF-1/ephrinB1 axis plays significant roles in the early stages of tooth injury. Further research is needed to fully understand the potential of targeting ephrinB1 as a regenerative pulp therapy.
[Mh] Termos MeSH primário: Dentina/metabolismo
Dentinogênese/fisiologia
Efrina-B1/metabolismo
Fator de Crescimento Insulin-Like I/metabolismo
Odontoblastos/metabolismo
[Mh] Termos MeSH secundário: Compostos de Alumínio/farmacologia
Animais
Compostos de Cálcio/farmacologia
Hidróxido de Cálcio/farmacologia
Polpa Dentária/metabolismo
Combinação de Medicamentos
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Modelos Animais
Óxidos/farmacologia
Transdução de Sinais
Silicatos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aluminum Compounds); 0 (Calcium Compounds); 0 (Drug Combinations); 0 (Ephrin-B1); 0 (Oxides); 0 (Silicates); 0 (mineral trioxide aggregate); 67763-96-6 (Insulin-Like Growth Factor I); PF5DZW74VN (Calcium Hydroxide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170511
[St] Status:MEDLINE
[do] DOI:10.1177/0022034517708572


  9 / 2662 MEDLINE  
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[PMID]:28365680
[Au] Autor:Wang F; Jiang Y; Huang X; Liu Q; Zhang Y; Luo W; Zhang F; Zhou P; Lin J; Zhang H
[Ad] Endereço:Chongqing Key Laboratory for Oral Diseases and Biomedical Sciences, the Affiliated Hospital of Stomatology of Chongqing Medical University, Chongqing, China.
[Ti] Título:Pro-Inflammatory Cytokine TNF-α Attenuates BMP9-Induced Osteo/ Odontoblastic Differentiation of the Stem Cells of Dental Apical Papilla (SCAPs).
[So] Source:Cell Physiol Biochem;41(5):1725-1735, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Periapical periodontitis is a common oral disease caused by bacterial invasion of the tooth pulp, which usually leads to local release of pro-inflammatory cytokines and osteolytic lesion. This study is intended to examine the effect of TNF-α on BMP9-induced osteogenic differentiation of the stem cells of dental apical papilla (SCAPs). METHODS: Rat model of periapical periodontitis was established. TNF-α expression was assessed. Osteogenic markers and ectopic bone formation in iSCAPs were analyzed upon BMP9 and TNF-α treatment. RESULTS: Periapical periodontitis was successfully established in rat immature permanent teeth with periapical lesions, in which TNF-α was shown to release during the inflammatory phase. BMP9-induced alkaline phosphatase activity, the expression of osteocalcin and osteopontin, and matrix mineralization in iSCAPs were inhibited by TNF-α in a dose-dependent fashion, although increased AdBMP9 partially overcame TNF-α inhibition. Furthermore, high concentration of TNF-α effectively inhibited BMP9-induced ectopic bone formation in vivo. CONCLUSION: TNF-α plays an important role in periapical bone defect during the inflammatory phase and inhibits BMP9-induced osteoblastic differentiation of iSCAPs, which can be partially reversed by high levels of BMP9. Therefore, BMP9 may be further explored as a potent osteogenic factor to improve osteo/odontogenic differentiation in tooth regeneration in chronic inflammation conditions.
[Mh] Termos MeSH primário: Diferenciação Celular
Fator 2 de Diferenciação de Crescimento/metabolismo
Odontoblastos/metabolismo
Periodontite Periapical/metabolismo
Células-Tronco/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Fosfatase Alcalina/biossíntese
Animais
Indução Enzimática
Masculino
Odontoblastos/patologia
Periodontite Periapical/patologia
Ratos
Ratos Sprague-Dawley
Células-Tronco/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Growth Differentiation Factor 2); 0 (Tumor Necrosis Factor-alpha); EC 3.1.3.1 (Alkaline Phosphatase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170623
[Lr] Data última revisão:
170623
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170403
[St] Status:MEDLINE
[do] DOI:10.1159/000471865


  10 / 2662 MEDLINE  
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[PMID]:28355287
[Au] Autor:Liao X; Feng B; Zhang D; Liu P; Zhou X; Li R; Ye L
[Ad] Endereço:State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
[Ti] Título:The Sirt6 gene: Does it play a role in tooth development?
[So] Source:PLoS One;12(3):e0174255, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dental Mesenchymal Cells (DMCs) are known to play a role in tooth development as well as in the repair and regeneration of dental tissue. A large number of signaling molecules regulate the proliferation and differentiation of DMC, though the underlying mechanisms are still not fully understood. Sirtuin-6 (SIRT6), a key regulator of aging, can exert an impact on embryonic stem cell (ESC) differentiation. The experimental deletion of Sirt6 in mouse bone marrow cells has been found to have an inhibiting impact on the bone mineral density and the osteogenic differentiation of these cells. The possible role of Sirt6 in tooth development, however, has at present remained largely unexplored. In the present study, we found that SIRT6 had no effect on tooth development before birth. However, Sirt6 gene deletion in knockout mice did have two post-natal impacts: a delay in tooth eruption and sluggishness in the development of dental roots. We propose an explanation of the possible molecular basis of the changes observed in Sirt6-/- mice. SIRT6 is expressed in mouse odontoblasts. Sirt6 deletion enhanced the proliferation of DMCs, as well as their capacity for adipogenic differentiation. On the other hand, it inhibited their capacity for in vitro osteogenic/chondrogenic differentiation. Further studies suggested that other factors may mediate the role of Sirt6 in odontogenesis. These include the nuclear factor kappa B (NF-κB), p38 mitogen-activated protein kinase (p38-MAPK), extracellular regulated MAP kinase (ERK) pathways and the mitochondrial energy. We demonstrated that Sirt6 plays a role in tooth root formation and confirmed that SIRT6 is necessary for DMC differentiation as well as for the development of the tooth root and for eventual tooth eruption. These results establish a new link between SIRT6 and tooth development.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica no Desenvolvimento
Células Mesenquimais Estromais/metabolismo
Dente Molar/metabolismo
Odontoblastos/metabolismo
Sirtuínas/genética
Raiz Dentária/metabolismo
[Mh] Termos MeSH secundário: Adipócitos/citologia
Adipócitos/metabolismo
Animais
Animais Recém-Nascidos
Diferenciação Celular
Embrião de Mamíferos
MAP Quinases Reguladas por Sinal Extracelular/genética
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Células Mesenquimais Estromais/citologia
Camundongos
Camundongos Knockout
Dente Molar/crescimento & desenvolvimento
NF-kappa B/genética
NF-kappa B/metabolismo
Odontoblastos/citologia
Odontogênese/genética
Transdução de Sinais
Sirtuínas/deficiência
Erupção Dentária/genética
Raiz Dentária/crescimento & desenvolvimento
Proteínas Quinases p38 Ativadas por Mitógeno/genética
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); EC 2.4.2.31 (Sirt6 protein, mouse); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 3.5.1.- (Sirtuins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170330
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0174255



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