TGF‐beta1 and TGFBR1 are Expressed in Ameloblasts and Promote MMP20 Expression

Gao, Yuguang; Li, Dongliang; Han, Tae-Ho; Sun, Yan; Zhang, Juanjuan

doi:10.1002/ar.20901

Cited by 36 publications

(37 citation statements)

References 24 publications

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“…In contrast, Gao et al (2009) showed that for ALCs, TGF-β1 did not induce KLK4 expression but did induce MMP20 expression. In their study, MMP20 and KLK4 transcript levels were assessed by performing reverse transcription PCR with scanning of the resulting bands for quantification of gene expression.…”

Section: Discussionmentioning

confidence: 83%

Fluoride Affects Enamel Protein Content via TGF-β1-mediated KLK4 Inhibition

Suzuki¹,

Shin²,

Simmer

et al. 2014

J Dent Res

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Dental fluorosis is caused by chronic high-level fluoride (F -) exposure during enamel development, and fluorosed enamel has a higher than normal protein content. Matrix metalloproteinase 20 cleaves enamel matrix proteins during the secretory stage, and KLK4 further cleaves these proteins during the maturation stage so that the proteins can be reabsorbed from the hardening enamel. We show that transforming growth factor β1 (TGF-β1) can induce Klk4 expression, and we examine the effect of F -on TGF-β1 and KLK4 expression. We found that in vivo F -inhibits Klk4 but not Mmp20 transcript levels. LacZ-C57BL/6-Klk4 +/LacZ mice have LacZ inserted in frame at the Klk4 translation initiation site so that the endogenous Klk4 promoter drives LacZ expression in the same temporal/spatial way as it does for Klk4. KLK4 protein levels in rat enamel and β-galactosidase staining in LacZ-C57BL/6-Klk4 +/LacZ mouse enamel were both significantly reduced by F -treatment. Since TGF-β1 induces KLK4 expression, we tested and found that F -significantly reduced Tgf-β1 transcript levels in rat enamel organ. These data suggest that F --mediated downregulation of TGF-β1 expression contributes to reduced KLK4 protein levels in fluorosed enamel and provides an explanation for why fluorosed enamel has a higher than normal protein content.

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Section: Discussionmentioning

confidence: 83%

Fluoride Affects Enamel Protein Content via TGF-β1-mediated KLK4 Inhibition

Suzuki¹,

Shin²,

Simmer

et al. 2014

J Dent Res

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“…is expressed in ameloblasts of developing enamel (Gao et al, 2009). Interestingly, the tooth development in TGF-b1 mutant mice is unaffected, which could be partially due to rescue by maternal TGF-b1 (D'Souza and Litz, 1995).…”

Section: -Fold) In the Enamel Organs Of Itgb6mentioning

confidence: 99%

Critical role for αvβ6 integrin in enamel biomineralization

Mohazab

Koivisto

Jiang

et al. 2012

Journal of Cell Science

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SummaryTooth enamel has the highest degree of biomineralization of all vertebrate hard tissues. During the secretory stage of enamel formation, ameloblasts deposit an extracellular matrix that is in direct contact with the ameloblast plasma membrane. Although it is known that integrins mediate cell-matrix adhesion and regulate cell signaling in most cell types, the receptors that regulate ameloblast adhesion and matrix production are not well characterized. We hypothesized that avb6 integrin is expressed in ameloblasts where it regulates biomineralization of enamel. Human and mouse ameloblasts were found to express both b6 integrin mRNA and protein. The maxillary incisors of Itgb6 2/2 mice lacked yellow pigment and their mandibular incisors appeared chalky and rounded. Molars of Itgb6 2/2 mice showed signs of reduced mineralization and severe attrition. The mineral-to-protein ratio in the incisors was significantly reduced in Itgb6 2/2 enamel, mimicking hypomineralized amelogenesis imperfecta. Interestingly, amelogenin-rich extracellular matrix abnormally accumulated between the ameloblast layer of Itgb6 2/2 mouse incisors and the forming enamel surface, and also between ameloblasts. This accumulation was related to increased synthesis of amelogenin, rather than to reduced removal of the matrix proteins. This was confirmed in cultured ameloblast-like cells, in which avb6 integrin was not an endocytosis receptor for amelogenins, although it participated in cell adhesion on this matrix indirectly via endogenously produced matrix proteins. In summary, integrin avb6 is expressed by ameloblasts and it plays a crucial role in regulating amelogenin deposition and/or turnover and subsequent enamel biomineralization.

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“…Reportedly, TGF-β is present in the inner enamel epithelium and cervical loop, is involved in tooth morphogenesis, regulates secretory ameloblast differentiation 14) , and promotes amelogenin and enamelysin secretion 20), 21) . In our study, TGF-β-R1, Smad3, and p-Smad3 showed strong or strongest positive reactions in the inner enamel epithelium, cervical loop, and secretory ameloblasts, and the reactions of Smad3 and p-Smad3 were particularly strong in the cell nuclei in the inner enamel epithelium.…”

Section: Ameloblasts and The Wnt And Tgf-β β β β β Signaling Pathwaysmentioning

confidence: 99%

Immunolocalization of Axin2 and p-Smad3 in Developing Rat Molar Germ

Moriguchi

Yamada

Miake

et al. 2012

J. Hard Tissue Biology.

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Wnt is involved in odontoblast and ameloblast differentiation and matrix protein expression in dentin and enamel, but there have been only a few reports on Axin2 in the Wnt signaling pathway. Axin2 promotes Smad3 activation in the transforming growth factor beta (TGF-ß) signaling pathway, and the presence of crosstalk between the Wnt and TGF-ß signaling pathways has been reported, but there have been no reports on that in odontogenic cells. Thus, we examined immunohistochemically the factors in the 2 signaling pathways using serial sections of rat first molar germ at embryonic day 19 and 10 days after birth to investigate whether there is cross-talk between the 2 signaling pathways through Axin2 and Smad3. Factors in the Wnt signaling pathway: Wnt10, Dishevelled (Dvl), and Axin2, and those in the TGF-ß signaling pathway: TGF-ß receptor 1 (TGF-ß-R1), Smad3, and its active type, phosphorylated Smad3 (p-Smad3), showed similar immunoreactions; in detail, odontoblasts possessing secretory function, rather than dental papilla cells and preodontoblasts, and secretorystage ameloblasts, rather than inner enamel epithelium, showed stronger reactions, whereas the reaction of maturation-stage ameloblasts was very weak. In addition, the reaction of Axin2 was completely consistent with that of pSmad3, and odontoblasts and secretory ameloblasts showed the strongest positive reactions. Accordingly, it was suggested that the TGF-ß signaling pathway as well as Dvl-and Axin2-mediated Wnt10 signaling pathway may are involved in odontoblast and ameloblast differentiation and the secretory function of these cells. In addition, the reaction of Axin2 was completely consistent with that of pSmad3, and odontoblasts and secretory ameloblasts showed the strongest positive reactions, suggesting that a cross-talk between the 2 signaling pathways through Axin2 and Smad3 may be involved in the odontoblast and ameloblast differentiation and secretory function of these cells.

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TGF‐beta1 and TGFBR1 are Expressed in Ameloblasts and Promote MMP20 Expression

Cited by 36 publications

References 24 publications

Fluoride Affects Enamel Protein Content via TGF-β1-mediated KLK4 Inhibition

Fluoride Affects Enamel Protein Content via TGF-β1-mediated KLK4 Inhibition

Critical role for αvβ6 integrin in enamel biomineralization

Immunolocalization of Axin2 and p-Smad3 in Developing Rat Molar Germ

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