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Pesquisa : G07.345.500.325.377.750.190 [Categoria DeCS]
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[PMID]:28732182
[Au] Autor:Furukawa Y; Haruyama N; Nikaido M; Nakanishi M; Ryu N; Oh-Hora M; Kuremoto K; Yoshizaki K; Takano Y; Takahashi I
[Ad] Endereço:1 Section of Orthodontics and Dentofacial Orthopedics, Division of Oral Health, Growth, and Development, Faculty of Dental Science, Kyushu University, Fukuoka, Japan.
[Ti] Título:Stim1 Regulates Enamel Mineralization and Ameloblast Modulation.
[So] Source:J Dent Res;96(12):1422-1429, 2017 Nov.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Loss-of-function mutations in the Ca release-activated Ca channel genes ORAI1 and STIM1 abolish store-operated Ca entry (SOCE) and result in ectodermal dysplasia with amelogenesis imperfecta. However, because of the limited availability of patient tissue, analyses of enamel mineralization or possible changes in ameloblast function or morphology have not been possible. Here, we generated mice with ectodermal tissue-specific deletion of Stim1 ( Stim1 cKO [conditional knockout]), Stim2 ( Stim2 cKO), and Stim1 and Stim2 ( Stim1/2 cKO) and analyzed their enamel phenotypes as compared with those of control ( Stim1/2 ) animals. Ablation of Stim1 and Stim1/2 but not Stim2 expression resulted in chalky enamel and severe attrition at the incisor tips and molar cusps. Stim1 and Stim1/2 cKO, but not Stim2 cKO, demonstrated inferior enamel mineralization with impaired structural integrity, whereas the shape of the teeth and enamel thickness appeared to be normal in all animals. The gene expression levels of the enamel matrix proteins Amelx and Ambn and the enamel matrix proteases Mmp20 and Klk4 were not altered by the abrogation of SOCE in Stim1/2 cKO mice. The morphology of ameloblasts during the secretory and maturation stages was not significantly altered in either the incisors or molars of the cKO animals. However, in Stim1 and Stim1/2 cKO incisors, the alternating modulation of maturation-stage ameloblasts between the smooth- and ruffle-ended cell types continued beyond the regular cycle and extended to the areas corresponding to the zone of postmodulation ameloblasts in the teeth of control animals. These results indicate that SOCE is essential for proper enamel mineralization, in which Stim1 plays a critical role during the maturation process.
[Mh] Termos MeSH primário: Ameloblastos/fisiologia
Amelogênese/genética
Molécula 1 de Interação Estromal/genética
[Mh] Termos MeSH secundário: Amelogênese Imperfeita/genética
Animais
Canais de Cálcio/genética
Proteínas do Esmalte Dentário/genética
Genótipo
Imuno-Histoquímica
Camundongos
Camundongos Transgênicos
Microscopia Eletrônica de Varredura
Fenótipo
Reação em Cadeia da Polimerase
Microtomografia por Raio-X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); 0 (Dental Enamel Proteins); 0 (Stromal Interaction Molecule 1); 0 (enamel matrix proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE
[do] DOI:10.1177/0022034517719872


  2 / 1060 MEDLINE  
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[PMID]:28644741
[Au] Autor:Zheng X; Goodwin AF; Tian H; Jheon AH; Klein OD
[Ad] Endereço:1 Department of Stomatology, Peking University Third Hospital, Beijing, China.
[Ti] Título:Ras Signaling Regulates Stem Cells and Amelogenesis in the Mouse Incisor.
[So] Source:J Dent Res;96(12):1438-1444, 2017 Nov.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The role of Ras signaling during tooth development is poorly understood. Ras proteins-which are activated by many upstream pathways, including receptor tyrosine kinase cascades-signal through multiple effectors, such as the mitogen-activated protein kinase (MAPK) and PI3K pathways. Here, we utilized the mouse incisor as a model to study how the MAPK and PI3K pathways regulate dental epithelial stem cells and amelogenesis. The rodent incisor-which grows continuously throughout the life of the animal due to the presence of epithelial and mesenchymal stem cells-provides a model for the study of ectodermal organ renewal and regeneration. Utilizing models of Ras dysregulation as well as inhibitors of the MAPK and PI3K pathways, we found that MAPK and PI3K regulate dental epithelial stem cell activity, transit-amplifying cell proliferation, and enamel formation in the mouse incisor.
[Mh] Termos MeSH primário: Amelogênese/fisiologia
Transdução de Sinais/fisiologia
Células-Tronco/fisiologia
Proteínas ras/metabolismo
[Mh] Termos MeSH secundário: Animais
Benzamidas/farmacologia
Proliferação Celular
Difenilamina/análogos & derivados
Difenilamina/farmacologia
Imunofluorescência
Incisivo
Indazóis/farmacologia
Camundongos
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Modelos Animais
Fosfatidilinositol 3-Quinases/metabolismo
Fosforilação
Sulfonamidas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(1H-indazol-4-yl)-6-(4-methanesulfonylpiperazin-1-ylmethyl)-4-morpholin-4-ylthieno(3,2-d)pyrimidine); 0 (Benzamides); 0 (Indazoles); 0 (PD 0325901); 0 (Sulfonamides); 9N3CBB0BIQ (Diphenylamine); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.137 (Pik3cd protein, mouse); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.6.5.2 (ras Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170624
[St] Status:MEDLINE
[do] DOI:10.1177/0022034517717255


  3 / 1060 MEDLINE  
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[PMID]:28221098
[Au] Autor:Bronckers AL
[Ad] Endereço:1 Department of Oral Cell Biology, Academic Centre for Dentistry Amsterdam (ACTA), University of Amsterdam and VU University Amsterdam, MOVE Research Institute, Amsterdam, Netherlands.
[Ti] Título:Ion Transport by Ameloblasts during Amelogenesis.
[So] Source:J Dent Res;96(3):243-253, 2017 Mar.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hypomineralization of developing enamel is associated with changes in ameloblast modulation during the maturation stage. Modulation (or pH cycling) involves the cyclic transformation of ruffle-ended (RE) ameloblasts facing slightly acidic enamel into smooth-ended (SE) ameloblasts near pH-neutral enamel. The mechanism of ameloblast modulation is not clear. Failure of ameloblasts of Cftr-null and anion exchanger 2 ( Ae2)-null mice to transport Cl into enamel acidifies enamel, prevents modulation, and reduces mineralization. It suggests that pH regulation is critical for modulation and for completion of enamel mineralization. This report presents a review of the major types of transmembrane molecules that ameloblasts express to transport calcium to form crystals and bicarbonates to regulate pH. The type of transporter depends on the developmental stage. Modulation is proposed to be driven by the pH of enamel fluid and the compositional and/or physicochemical changes that result from increased acidity, which may turn RE ameloblasts into SE mode. Amelogenins delay outgrowth of crystals and keep the intercrystalline space open for diffusion of mineral ions into complete depth of enamel. Modulation enables stepwise removal of amelogenins from the crystal surface, their degradation, and removal from the enamel. Removal of matrix allows slow expansion of crystals. Modulation also reduces the stress that ameloblasts experience when exposed to high acid levels generated by mineral formation or by increased intracellular Ca . By cyclically interrupting Ca transport by RE ameloblasts and their transformation into SE ameloblasts, proton production ceases shortly and enables the ameloblasts to recover. Modulation also improves enamel crystal quality by selectively dissolving immature Ca -poor crystals, removing impurities as Mg and carbonates, and recrystallizing into more acid-resistant crystals.
[Mh] Termos MeSH primário: Ameloblastos/fisiologia
Amelogênese/fisiologia
Transporte de Íons/fisiologia
[Mh] Termos MeSH secundário: Ameloblastos/metabolismo
Animais
Antiportadores de Cloreto-Bicarbonato/fisiologia
Regulador de Condutância Transmembrana em Fibrose Cística/fisiologia
Esmalte Dentário/crescimento & desenvolvimento
Concentração de Íons de Hidrogênio
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Chloride-Bicarbonate Antiporters); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170531
[Lr] Data última revisão:
170531
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE
[do] DOI:10.1177/0022034516681768


  4 / 1060 MEDLINE  
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[PMID]:28113034
[Au] Autor:Kwak SY; Litman A; Margolis HC; Yamakoshi Y; Simmer JP
[Ad] Endereço:1 Center for Biomineralization, Department of Applied Oral Sciences, The Forsyth Institute, Cambridge, MA, USA.
[Ti] Título:Biomimetic Enamel Regeneration Mediated by Leucine-Rich Amelogenin Peptide.
[So] Source:J Dent Res;96(5):524-530, 2017 May.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We report here a novel biomimetic approach to the regeneration of human enamel. The approach combines the use of inorganic pyrophosphate (PP ) to control the onset and rate of enamel regeneration and the use of leucine-rich amelogenin peptide (LRAP), a nonphosphorylated 56-amino acid alternative splice product of amelogenin, to regulate the shape and orientation of growing enamel crystals. This study builds on our previous findings that show LRAP can effectively guide the formation of ordered arrays of needle-like hydroxyapatite (HA) crystals in vitro and on the known role mineralization inhibitors, like PP , play in the regulation of mineralized tissue formation. Acid-etched enamel surfaces of extracted human molars, cut perpendicular or parallel to the direction of the enamel rods, were exposed to a PP -stabilized supersaturated calcium phosphate (CaP) solution containing 0 to 0.06 mg/mL LRAP for 20 h. In the absence of LRAP, PP inhibition was reversed by the presence of etched enamel surfaces and led to the formation of large, randomly distributed plate-like HA crystals that were weakly attached, regardless of rod orientation. In the presence of 0.04 mg/mL LRAP, however, densely packed mineral layers, comprising bundles of small needle-like HA crystals, formed on etched surfaces that were cut perpendicular to the enamel rods. These crystals were strongly attached, and their arrangement reflected to a significant degree the underlying enamel prism pattern. In contrast, under the same conditions with LRAP, little to no crystal formation was found on enamel surfaces that were cut parallel to the direction of the enamel rods. These results suggest that LRAP preferentially interacts with ab surfaces of mature enamel crystals, inhibiting their directional growth, thus selectively promoting linear growth along the c-axis of enamel crystals. The present findings demonstrate a potential for the development of a new approach to regenerate enamel structure and properties.
[Mh] Termos MeSH primário: Amelogênese/efeitos dos fármacos
Biomimética
Proteínas do Esmalte Dentário/farmacologia
[Mh] Termos MeSH secundário: Ataque Ácido Dentário
Animais
Fosfatos de Cálcio/farmacologia
Cristalização
Seres Humanos
Concentração de Íons de Hidrogênio
Técnicas In Vitro
Microscopia Eletrônica de Varredura
Propriedades de Superfície
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Phosphates); 0 (Dental Enamel Proteins); 0 (leucine-rich amelogenin peptide); 97Z1WI3NDX (calcium phosphate)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170124
[St] Status:MEDLINE
[do] DOI:10.1177/0022034516688659


  5 / 1060 MEDLINE  
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[PMID]:28030993
[Au] Autor:Nirvani M; Khuu C; Utheim TP; Hollingen HS; Amundsen SF; Sand LP; Sehic A
[Ad] Endereço:a Department of Oral Biology, Faculty of Dentistry , University of Oslo , Oslo , Norway.
[Ti] Título:Circadian rhythms and gene expression during mouse molar tooth development.
[So] Source:Acta Odontol Scand;75(2):144-153, 2017 Mar.
[Is] ISSN:1502-3850
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Incremental markings in dental enamel suggest that the circadian clock may influence the molecular underpinnings orchestrating enamel formation. The aim of this study was to investigate whether the genes and microRNAs (miRNAs) oscillate in a circadian pattern during tooth and enamel development. MATERIAL AND METHODS: Comparative gene and miRNA expression profiling of the first mandibular molar tooth germ isolated at different time-points during the light and night period was performed using microarrays and validated using real-time RT-PCR. Bioinformatic analysis was carried out using Ingenuity Pathway Analysis (IPA), and TargetScan software was used in order to identify computationally predicted miRNA-mRNA target relationships. RESULTS: In total, 439 genes and 32 miRNAs exhibited significantly different (p < 0.05) levels of expression in the light phase compared with the night phase tooth germs. Genes involved in enamel formation, i.e. Amelx, Ambn, Amtn, and Odam, oscillated in a circadian pattern. Furthermore, the circadian clock genes, in particular Clock and Bmal1, oscillated in mouse molar tooth germ during 24-h intervals. The expression of Clock and Bmal1 was inversely correlated with the expression of miR-182 and miR-141, respectively. CONCLUSIONS: MiRNAs, including miR-182 and miR-141, are involved in the control of peripheral circadian rhythms in the developing tooth by regulating the expression of genes coding for circadian transcription factors such as CLOCK and BMAL1. Regulation of circadian rhythms may be important for enamel phenotype, and the morphology of dental enamel may vary between individuals due to differences in circadian profiles.
[Mh] Termos MeSH primário: Ritmo Circadiano
Regulação da Expressão Gênica no Desenvolvimento
Dente Molar/crescimento & desenvolvimento
Calcificação de Dente/genética
Germe de Dente/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Amelogênese
Animais
Esmalte Dentário/crescimento & desenvolvimento
Camundongos
MicroRNAs
Dente Molar/química
Odontogênese/fisiologia
RNA Mensageiro/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (RNA, Messenger)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:161230
[St] Status:MEDLINE
[do] DOI:10.1080/00016357.2016.1271999


  6 / 1060 MEDLINE  
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[PMID]:27959403
[Au] Autor:Li Z; Chen G; Yang Y; Guo W; Tian W
[Ad] Endereço:National Engineering Laboratory for Oral Regenerative Medicine, West China School of Stomatology, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
[Ti] Título:Bcl11b regulates enamel matrix protein expression and dental epithelial cell differentiation during rat tooth development.
[So] Source:Mol Med Rep;15(1):297-304, 2017 Jan.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Amelogenesis, beginning with thickened epithelial aggregation and ending with highly mineralized enamel formation, is a process mediated by a complex signaling network that involves several molecules, including growth and transcription factors. During early tooth development, the transcription factor B­cell CLL/lymphoma 11B (Bcl11b) participates in dental epithelial cell proliferation and differentiation. However, whether it affects the postnatal regulation of enamel matrix protein expression and ameloblast differentiation remains unclear. To clarify the role of Bcl11b in enamel development, the present study initially detected the protein expression levels of Bcl11b during tooth development using immunohistochemistry, from the embryonic lamina stage to the postnatal period, and demonstrated that Bcl11b is predominantly restricted to cervical loop epithelial cells at the cap and bell stages, whereas expression is reduced in ameloblasts. Notably, the expression pattern of Bcl11b during tooth development differed between rats and mice. Knockdown of Bcl11b by specific small interfering RNA attenuated the expression of enamel­associated genes, including amelogenin, X­linked (Amelx), ameloblastin (Ambn), enamelin (Enam), kallikrein related peptidase 4 (Klk4), matrix metallopeptidase 20 and Msh homeobox 2 (Msx2). Chromatin immunoprecipitation assay verified that Msx2 was a transcriptional target of Bcl11b. However, overexpression of Msx2 resulted in downregulation of enamel­associated genes, including Ambn, Amelx, Enam and Klk4. The present study suggested that Bcl11b serves a potentially important role in the regulation of ameloblast differentiation and enamel matrix protein expression. In addition, a complex feedback regulatory network may exist between Bcl11b and Msx2.
[Mh] Termos MeSH primário: Proteínas do Esmalte Dentário/genética
Regulação da Expressão Gênica no Desenvolvimento
Proteínas Repressoras/genética
Dente/crescimento & desenvolvimento
Proteínas Supressoras de Tumor/genética
[Mh] Termos MeSH secundário: Ameloblastos/citologia
Ameloblastos/metabolismo
Amelogênese
Animais
Diferenciação Celular
Linhagem Celular
Células Epiteliais/citologia
Células Epiteliais/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Odontogênese
Interferência de RNA
RNA Interferente Pequeno/genética
Ratos
Ratos Sprague-Dawley
Proteínas Repressoras/análise
Dente/metabolismo
Proteínas Supressoras de Tumor/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BCL11B protein, rat); 0 (Dental Enamel Proteins); 0 (RNA, Small Interfering); 0 (Repressor Proteins); 0 (Tumor Suppressor Proteins); 0 (enamel matrix proteins)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161214
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2016.6030


  7 / 1060 MEDLINE  
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[PMID]:27693231
[Au] Autor:Parry DA; Smith CE; El-Sayed W; Poulter JA; Shore RC; Logan CV; Mogi C; Sato K; Okajima F; Harada A; Zhang H; Koruyucu M; Seymen F; Hu JC; Simmer JP; Ahmed M; Jafri H; Johnson CA; Inglehearn CF; Mighell AJ
[Ad] Endereço:Leeds Institute of Biomedical and Clinical Sciences, University of Leeds, St. James's University Hospital, Leeds LS9 7TF, UK; Centre for Genomic and Experimental Medicine, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh EH4 2XU, UK.
[Ti] Título:Mutations in the pH-Sensing G-protein-Coupled Receptor GPR68 Cause Amelogenesis Imperfecta.
[So] Source:Am J Hum Genet;99(4):984-990, 2016 Oct 06.
[Is] ISSN:1537-6605
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Amelogenesis is the process of dental enamel formation, leading to the deposition of the hardest tissue in the human body. This process requires the intricate regulation of ion transport and controlled changes to the pH of the developing enamel matrix. The means by which the enamel organ regulates pH during amelogenesis is largely unknown. We identified rare homozygous variants in GPR68 in three families with amelogenesis imperfecta, a genetically and phenotypically heterogeneous group of inherited conditions associated with abnormal enamel formation. Each of these homozygous variants (a large in-frame deletion, a frameshift deletion, and a missense variant) were predicted to result in loss of function. GPR68 encodes a proton-sensing G-protein-coupled receptor with sensitivity in the pH range that occurs in the developing enamel matrix during amelogenesis. Immunohistochemistry of rat mandibles confirmed localization of GPR68 in the enamel organ at all stages of amelogenesis. Our data identify a role for GPR68 as a proton sensor that is required for proper enamel formation.
[Mh] Termos MeSH primário: Amelogênese Imperfeita/genética
Mutação
Receptores Acoplados a Proteínas-G/genética
[Mh] Termos MeSH secundário: Amelogênese/genética
Animais
Sequência de Bases
Esmalte Dentário/crescimento & desenvolvimento
Esmalte Dentário/patologia
Feminino
Homozigoto
Seres Humanos
Concentração de Íons de Hidrogênio
Masculino
Linhagem
Ratos
Receptores Acoplados a Proteínas-G/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GPR68 protein, human); 0 (GPR68 protein, rat); 0 (Receptors, G-Protein-Coupled)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170524
[Lr] Data última revisão:
170524
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161004
[St] Status:MEDLINE


  8 / 1060 MEDLINE  
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[PMID]:27684650
[Au] Autor:Jedeon K; Loiodice S; Salhi K; Le Normand M; Houari S; Chaloyard J; Berdal A; Babajko S
[Ad] Endereço:Centre de Recherche des Cordeliers (K.J., S.L., K.S., M.L.N., S.H., J.C., A.B., S.B.), INSERM Unité Mixte de Recherche en Santé 1138, Université Paris-Descartes, Université Pierre et Marie Curie-Paris, Paris Laboratory of Molecular Oral Pathophysiology, and Unité de Formation et de Recherche d'Odont
[Ti] Título:Androgen Receptor Involvement in Rat Amelogenesis: An Additional Way for Endocrine-Disrupting Chemicals to Affect Enamel Synthesis.
[So] Source:Endocrinology;157(11):4287-4296, 2016 Nov.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endocrine-disrupting chemicals (EDCs) that interfere with the steroid axis can affect amelogenesis, leading to enamel hypomineralization similar to that of molar incisor hypomineralization, a recently described enamel disease. We investigated the sex steroid receptors that may mediate the effects of EDCs during rat amelogenesis. The expression of androgen receptor (AR), estrogen receptor (ER)-α, and progesterone receptor was dependent on the stage of ameloblast differentiation, whereas ERß remained undetectable. AR was the only receptor selectively expressed in ameloblasts involved in final enamel mineralization. AR nuclear translocation and induction of androgen-responsive element-containing promoter activity upon T treatment, demonstrated ameloblast responsiveness to androgens. T regulated the expression of genes involved in enamel mineralization such as KLK4, amelotin, SLC26A4, and SLC5A8 but not the expression of genes encoding matrix proteins, which determine enamel thickness. Vinclozolin and to a lesser extent bisphenol A, two antiandrogenic EDCs that cause enamel defects, counteracted the actions of T. In conclusion, we show, for the first time, the following: 1) ameloblasts express AR; 2) the androgen signaling pathway is involved in the enamel mineralization process; and 3) EDCs with antiandrogenic effects inhibit AR activity and preferentially affect amelogenesis in male rats. Their action, through the AR pathway, may specifically and irreversibly affect enamel, potentially leading to the use of dental defects as a biomarker of exposure to environmental pollutants. These results are consistent with the steroid hormones affecting ameloblasts, raising the issue of the hormonal influence on amelogenesis and possible sexual dimorphism in enamel quality.
[Mh] Termos MeSH primário: Ameloblastos/efeitos dos fármacos
Ameloblastos/metabolismo
Disruptores Endócrinos/toxicidade
[Mh] Termos MeSH secundário: Amelogênese/efeitos dos fármacos
Animais
Compostos Benzidrílicos/toxicidade
Linhagem Celular
Antiportadores de Cloreto-Bicarbonato/genética
Antiportadores de Cloreto-Bicarbonato/metabolismo
Esmalte Dentário/efeitos dos fármacos
Esmalte Dentário/metabolismo
Proteínas do Esmalte Dentário/genética
Proteínas do Esmalte Dentário/metabolismo
Imunofluorescência
Perfilação da Expressão Gênica
Calicreínas/genética
Calicreínas/metabolismo
Masculino
Transportadores de Ácidos Monocarboxílicos/genética
Transportadores de Ácidos Monocarboxílicos/metabolismo
Oxazóis/toxicidade
Fenóis/toxicidade
Ratos
Ratos Wistar
Receptores Androgênicos/genética
Receptores Androgênicos/metabolismo
Receptores Estrogênicos/genética
Receptores Estrogênicos/metabolismo
Receptores de Progesterona/genética
Receptores de Progesterona/metabolismo
Receptores de Esteroides/genética
Receptores de Esteroides/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amtn protein, rat); 0 (Benzhydryl Compounds); 0 (Chloride-Bicarbonate Antiporters); 0 (Dental Enamel Proteins); 0 (Endocrine Disruptors); 0 (Monocarboxylic Acid Transporters); 0 (Oxazoles); 0 (Phenols); 0 (Receptors, Androgen); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone); 0 (Receptors, Steroid); 0 (pendrin protein, rat); 0 (sodium-coupled monocarboxylate transporter 1, rat); EC 3.4.21.- (Kallikreins); EC 3.4.21.- (kallikrein 4); JJ258EZN1I (vinclozolin); MLT3645I99 (bisphenol A)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170519
[Lr] Data última revisão:
170519
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160930
[St] Status:MEDLINE


  9 / 1060 MEDLINE  
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[PMID]:27558264
[Au] Autor:Kwak SY; Yamakoshi Y; Simmer JP; Margolis HC
[Ad] Endereço:Center for Biomineralization, Department of Applied Oral Sciences, The Forsyth Institute, Cambridge, MA, USA.
[Ti] Título:MMP20 Proteolysis of Native Amelogenin Regulates Mineralization In Vitro.
[So] Source:J Dent Res;95(13):1511-1517, 2016 Dec.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent studies have shown that native phosphorylated full-length porcine amelogenin (P173) and its predominant cleavage product (P148) can inhibit spontaneous calcium phosphate formation in vitro by stabilizing an amorphous calcium phosphate (ACP) precursor phase. Since full-length amelogenin undergoes proteolysis by matrix metalloproteinase 20 (MMP20, enamelysin) soon after secretion, the present study was conducted to assess the effect of amelogenin proteolysis on calcium phosphate formation. Calcium and phosphate were sequentially added to protein solutions without and with added MMP20 (ratio = 200:1) under physiological-like conditions of ionic strength (163 mM) in 50 mM Tris-HCl (pH 7.4) at 37 °C. Protein degradation with time was assessed by gel-electrophoresis, and mineral products formed were characterized by transmission electron microscopy (TEM). MMP20 was found to cleave P173 to primarily generate P148, along with P162, P46-148, and P63/64-148. In sharp contrast, MMP20 did not cleave P148. In addition, the formation of well-aligned bundles of enamel-like hydroxyapatite (HA) crystals was promoted in the presence of P173 with added MMP20, while only ACP particles were seen in the absence of MMP20. Although P148 was found to have a somewhat lower capacity to stabilize ACP and prevent HA formation compared with P173 in the absence of MMP20, essentially no HA formation was observed in the presence of somewhat higher concentrations of P148 regardless of MMP20 addition, due to the lack of observed protein proteolysis. Present findings suggest that ACP transformation to ordered arrays of enamel crystals may be regulated in part by the proteolysis of full-length native amelogenin, while the predominant amelogenin degradation product in developing enamel (e.g., P148) primarily serves to prevent uncontrolled mineral formation during the secretory stage of amelogenesis.
[Mh] Termos MeSH primário: Amelogênese/fisiologia
Metaloproteinase 20 da Matriz/metabolismo
Proteólise
[Mh] Termos MeSH secundário: Amelogenina
Animais
Fosfatos de Cálcio
Eletroforese em Gel de Poliacrilamida
Concentração de Íons de Hidrogênio
Técnicas In Vitro
Microscopia Eletrônica de Transmissão
Fosforilação
Soluções
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amelogenin); 0 (Calcium Phosphates); 0 (Solutions); 97Z1WI3NDX (calcium phosphate); EC 3.4.24.- (Matrix Metalloproteinase 20)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:160826
[St] Status:MEDLINE


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[PMID]:27470066
[Au] Autor:Ma P; Yan W; Tian Y; He J; Brookes SJ; Wang X
[Ad] Endereço:1 Department of Oral Implantology, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.
[Ti] Título:The Importance of Serine Phosphorylation of Ameloblastin on Enamel Formation.
[So] Source:J Dent Res;95(12):1408-1414, 2016 Nov.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:FAM20C is a newly identified kinase on the secretory pathway responsible for the phosphorylation of serine residues in the Ser-x-Glu/pSer motifs in several enamel matrix proteins. Fam20C-knockout mice showed severe enamel defects very similar to those in the ameloblastin ( Ambn)-knockout mice, implying that phosphoserines may have a critical role in AMBN function. To test this hypothesis, we generated amelogenin ( Amel) promoter-driven Ambn-transgenic mice, in which Ser , Ser , and Ser were replaced by aspartic acid (designated as D-Tg) or alanines (designated as A-Tg). The negative charge of aspartic acid is believed to be able to mimic the phosphorylation state of serine, while alanine is a commonly used residue to substitute serine due to their similar structure. Using Western immunoblotting and quantitative polymerase chain reaction, the authors identified transgenic lines expressing transgenes somewhat higher (Tg+) or much higher (Tg++) than endogenous Ambn. The lower incisors collected from 7-d-old and 7-wk-old mice were analyzed by histology, scanning electron microscopy, immunohistochemistry, and Western immunoblotting to examine the morphology and microstructure changes in enamel, as well as the expression pattern of enamel matrix proteins. The A-Tg+ and A-Tg++ mice displayed severe enamel defects in spite of the expression level of transgenes, while the D-Tg+ and D-Tg++ mice showed minor to mild enamel defects, indicating that the D-Tg transgenes disturbed enamel formation less than the A-Tg transgenes did. Our results suggest that the phosphorylation state of serines is likely an essential component for the integrity of AMBN function.
[Mh] Termos MeSH primário: Amelogênese/fisiologia
Amelogenina/secreção
Proteínas de Ligação ao Cálcio/fisiologia
Proteínas do Esmalte Dentário/secreção
Proteínas da Matriz Extracelular/fisiologia
Serina/metabolismo
[Mh] Termos MeSH secundário: Amelogênese/genética
Amelogenina/genética
Animais
Western Blotting
Proteínas do Esmalte Dentário/genética
Matriz Extracelular/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Fosforilação
Reação em Cadeia da Polimerase
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ambn protein, mouse); 0 (Amelogenin); 0 (Calcium-Binding Proteins); 0 (Dental Enamel Proteins); 0 (Extracellular Matrix Proteins); 0 (FAM20C protein, mouse); 0 (enamel matrix proteins); 452VLY9402 (Serine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:160730
[St] Status:MEDLINE
[do] DOI:10.1177/0022034516661513



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