Distribution of transforming growth factor-β1-binding proteins and low-affinity receptors during odontoblast differentiation in the mouse

Cam, Y.; Lesot, Hervé; Colosetti, Pascal; Ruch, J V

doi:10.1016/s0003-9969(97)00017-4

Cited by 26 publications

(20 citation statements)

References 25 publications

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“…Among small leucine-rich proteoglycans, decorin and biglycan have been well characterized for their presence in the tooth. In mouse teeth, decorin was localized in odontoblasts, predentin, and dentin and biglycan in odontoblasts and predentin (37). In vitro studies have implied that decorin and biglycan play a crucial role in fibril growth and assembly.…”

Section: Discussionmentioning

confidence: 99%

Another Consequence of Severe Lupus: Invasive Fungal Disease

Barber

Barnabe

2012

J Rheumatol

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Dentin sialophosphoprotein (Dspp) is mainly expressed in teeth by the odontoblasts and preameloblasts. The Dspp mRNA is translated into a single protein, Dspp, and cleaved into two peptides, dentin sialoprotein and dentin phosphoprotein, that are localized within the dentin matrix. Recently, mutations in this gene were identified in human dentinogenesis imperfecta II (Online Mendelian Inheritance in Man (OMIM) accession number 125490) and in dentin dysplasia II (OMIM accession number 125420) syndromes. Herein, we report the generation of Dspp-null mice that develop tooth defects similar to human dentinogenesis imperfecta III with enlarged pulp chambers, increased width of predentin zone, hypomineralization, and pulp exposure. Electron microscopy revealed an irregular mineralization front and a lack of calcospherites coalescence in the dentin. Interestingly, the levels of biglycan and decorin, small leucine-rich proteoglycans, were increased in the widened predentin zone and in void spaces among the calcospherites in the dentin of null teeth. These enhanced levels correlate well with the defective regions in mineralization and further indicate that these molecules may adversely affect the dentin mineralization process by interfering with coalescence of calcospherites. Overall, our results identify a crucial role for Dspp in orchestrating the events essential during dentin mineralization, including potential regulation of proteoglycan levels.

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Section: Discussionmentioning

confidence: 99%

Another Consequence of Severe Lupus: Invasive Fungal Disease

Barber

Barnabe

2012

J Rheumatol

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“…The relative amount of BMP-2 and, to a lesser extent, BMP-4 increased from E17 to E19. Immunostaining showed that TGF ␤ 1 accumulated at the epithelial-mesenchymal junction where odontoblasts differentiated (Cam et al 1997;Kikuchi et al 2001). However, immunostaining for BMP-2 and -4 did not suggest any storage of these proteins at the epithelialmesenchymal junction in regions where odontoblasts had started to differentiate.…”

Section: Late Bell Stage and Cytodifferentiationmentioning

confidence: 99%

Immunolocalization of BMP-2/-4, FGF-4, and WNT10b in the Developing Mouse First Lower Molar

Nadiri

Kuchler‐Bopp

Haïkel

et al. 2004

J Histochem Cytochem.

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S U M M A R YIntercellular signaling controls all steps of odontogenesis. The purpose of this work was to immunolocalize in the developing mouse molar four molecules that play major roles during odontogenesis: BMP-2, -4, FGF-4, and WNT10b. BMP-2 and BMP-4 were detected in the epithelium and mesenchyme at the bud stage. Staining for BMP-2 markedly increased at the cap stage. The relative amount of BMP-4 strongly increased from E14 to E15. At E15, BMP-4 was detected in the internal part of the enamel knot where apoptosis was intense. In contrast to TGF ␤ 1, BMP-2 and -4 did not show accumulation at the epithelial-mesenchymal junction where the odontoblast started differentiation. When odontoblasts became functional, BMP-2 and BMP-4 were detected at the apical and basal poles of preameloblasts. BMP-2, which induces ameloblast differentiation in vitro , may also be involved physiologically. The decrease in FGF-4 from E14 to E15 supports a possible role for the growth factor in the control of mesenchymal cell proliferation. The relative amount of FGF-4 was maximal at E17. The subsequent decrease at E19 showed correlation with the withdrawal of odontoblasts and ameloblasts from the cell cycle. WNT10b might also stimulate cell proliferation. At E14-15, WNT10b was present in the mesenchyme and epithelium except for the enamel knot, where the mitotic activity was very low. At E19 there was a decreasing gradient of staining from the cervical loop where cells divide to the tip of the cusp in the inner dental epithelium where cells become postmitotic. The target cells for FGF-4 and WNT10b appeared different.

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“…Bars 50 µm the receptors. In our study, since TGF-β 1 visibly increases in the BM at odontogenic organs and is distributed along the periphery of tubular matrix-forming cells, dentinogenesis may be triggered by the activation of TGF-β 1 from the pericellular ECM, such as in the formation of a latent TGF-β complex in the BM (Ruch et al 1995;Cam et al 1997). This hypothesis is supported by biochemical analyses in which TGF-β 1 was detectable with antibodies specific for laminin-1 or type IV collagen in immunoprecipitates from cell lysates of dental papillae.…”

Section: Discussionmentioning

confidence: 67%

“…In embryos, the distribution of the TGF-β superfamily changes stage-specifically between the dental mesenchyme and epithelium (Thesleff and Sharpe 1997). TGF-β-binding protein or latencyassociated peptide has been revealed in the BM (Ruch et al 1995;Cam et al 1997) and TGF-β is localised in the BM (Pelton et al 1991). TGF-β has also been confirmed as being present in dentine (Finkelman et al 1990;Smith et al 1998) and it binds to the TGF-β type II receptors, which phosphorylate type I receptors as transductive signal pathways (Wrana et al 1994;Heldin et al 1997).…”

Section: Introductionmentioning

confidence: 99%

“…These do not resemble the BM but their function may be similar to that of the BM. A close association has been suggested between the BM, dentinogenesis and the TGF-β superfamily (Ruch et al 1995;Cam et al 1997;Thesleff and Sharpe 1997) but it is still poorly understood. To elucidate the role of the BM in dentinogenesis, we have examined, by means of our established system, the way in which inducible dentinogenesis depends on BM components or TGF-β 1 , together with an ECM-absorbed agar substratum that may have functions similar to the BM (Kikuchi et al 1996).…”

Section: Introductionmentioning

confidence: 99%

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Putative role of basement membrane for dentinogenesis in the mesenchyme of murine dental papillae in vitro

Kikuchi

Amano

Yamada

2001

Cell and Tissue Research

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In a new culture-conditioning system of agar-coated mesenchyme of isolated incisor dental papillae, dentinogenesis has been induced adjacent to an agar substratum that functions as a foothold for cell immobilisation. To elucidate the role of the basement membrane (BM) in dentinogenesis, we have examined the way in which dentinogenesis depends upon BM components or transforming growth factor (TGF)-beta1 in this system. At the mesenchymal-epithelial junction of odontogenic organs (cut incisor tooth germs), TGF-beta1 visibly increased in the BM during incubation. In isolated dental papillae, BM components were synthesised and deposited at aligned peripheral cells of the explants, together with an increasing amount of TGF-beta1. These components were not assembled into extracellular matrix (ECM)-absorbed agar adjacent to explants, although dentinogenesis proceeded in the presence of pericellular BM components associated with TGF-beta1. When signalling via TGF-beta type II receptors was blocked, neither ECM production nor dentinogenesis was observed but explants partially detached from the agar surface, presumably as a result of the suppressed production of ECM, since attachment was retained by pre-coating explants with artificial matrices. Rescue experiments showed that TGF-beta1 regulated dentinogenesis through ECM production. With regard to BM components, inducible dentinogenesis was Arg-Gly-Asp (RGD)-dependent. Thus, pericellular BM components associated with TGF-beta1 and an ECM-absorbed agar substratum, which affects dentinogenesis, synergistically play a role similar to that of BM components in vivo. The BM therefore serves as a structural meshwork that acts as a foothold for cell immobilisation; its components act as ligands for RGD-dependent cell adhesion and it stores TGF-beta1, which regulates ECM production.

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Distribution of transforming growth factor-β1-binding proteins and low-affinity receptors during odontoblast differentiation in the mouse

Cited by 26 publications

References 25 publications

Another Consequence of Severe Lupus: Invasive Fungal Disease

Another Consequence of Severe Lupus: Invasive Fungal Disease

Immunolocalization of BMP-2/-4, FGF-4, and WNT10b in the Developing Mouse First Lower Molar

Putative role of basement membrane for dentinogenesis in the mesenchyme of murine dental papillae in vitro

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