Enamel Matrix Derivative: A Review of Cellular Effects<i>In Vitro</i>and a Model of Molecular Arrangement and Functioning

Grandin, H. Michelle; Gemperli, Anja C.; Dard, Michel

doi:10.1089/ten.teb.2011.0365

Cited by 103 publications

(122 citation statements)

References 192 publications

(330 reference statements)

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“…These proteins are important in the development of acellular cementum, the periodontal ligament, and alveolar bone. EMD has a variety of biological effects in vitro , such as regeneration of mesenchymal and epithelial cells, enhancement of wound healing via extracellular matrix synthesis, and the regulation of molecules involved in bone remodeling 1 , 8 . Genome-wide microarray approach demonstrated that EMD causes substantial alternations in gene expression, with similar patterns observed in palatal and gingival fibroblasts 11 .…”

Section: Introductionmentioning

confidence: 99%

Novel biological activity of ameloblastin in enamel matrix derivative

et al. 2015

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Objective Enamel matrix derivative (EMD) is used clinically to promote periodontal tissue regeneration. However, the effects of EMD on gingival epithelial cells during regeneration of periodontal tissues are unclear. In this in vitro study, we purified ameloblastin from EMD and investigated its biological effects on epithelial cells.Material and Methods Bioactive fractions were purified from EMD by reversed-phase high-performance liquid chromatography using hydrophobic support with a C18 column. The mouse gingival epithelial cell line GE-1 and human oral squamous cell carcinoma line SCC-25 were treated with purified EMD fraction, and cell survival was assessed with a WST-1 assay. To identify the proteins in bioactive fractions of EMD, we used proteome analysis with two-dimensional gel electrophoresis followed by identification with liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis.Results Purified fractions from EMD suppressed proliferation of GE-1 and SCC-25. LC-MS/MS revealed that ameloblastin in EMD is the component responsible for inhibiting epithelial cell proliferation. The inhibitory effect of ameloblastin on the proliferation of GE-1 and SCC-25 was confirmed using recombinant protein.Conclusion The inhibitory effects of EMD on epithelial cell proliferation are caused by the biological activities of ameloblastin, which suggests that ameloblastin is involved in regulating epithelial downgrowth in periodontal tissues.

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Section: Introductionmentioning

confidence: 99%

Novel biological activity of ameloblastin in enamel matrix derivative

et al. 2015

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“…Emdogain consists of enamel matrix derivatives and the vehicle propylene glycol alginate (Institut Straumann, Basel, Switzerland) [1]. The local application of Emdogain has been shown to support skin wound healing [2], [3].…”

Section: Introductionmentioning

confidence: 99%

Emdogain-Regulated Gene Expression in Palatal Fibroblasts Requires TGF-βRI Kinase Signaling

et al. 2014

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Genome-wide microarrays have suggested that Emdogain regulates TGF-β target genes in gingival and palatal fibroblasts. However, definitive support for this contention and the extent to which TGF-β signaling contributes to the effects of Emdogain has remained elusive. We therefore studied the role of the TGF-β receptor I (TGF-βRI) kinase to mediate the effect of Emdogain on palatal fibroblasts. Palatal fibroblasts were exposed to Emdogain with and without the inhibitor for TGF-βRI kinase, SB431542. Emdogain caused 39 coding genes to be differentially expressed in palatal fibroblasts by microarray analysis (p<0.05; >10-fold). Importantly, in the presence of the TGF-βRI kinase inhibitor SB431542, Emdogain failed to cause any significant changes in gene expression. Consistent with this mechanism, three independent TGF-βRI kinase inhibitors and a TGF-β neutralizing antibody abrogated the increased expression of IL-11, a selected Emdogain target gene. The MAPK inhibitors SB203580 and U0126 lowered the impact of Emdogain on IL-11 expression. The data support that TGF-βRI kinase activity is necessary to mediate the effects of Emdogain on gene expression in vitro.

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“…More specifically, using recombinant AMELX and AMBN and transgenic mice that overexpressed EMPs and their splicing forms, previous studies have demonstrated that EMPs control cell adhesion, proliferation, polarity, commitment, differentiation and act on key-cellular pathways [18]–[22]. To date, nearly all the cells of dental-periodontal, epidermal and bone compartments have been found to respond to EMPs (for review, [23]). Transgenic mouse studies indicated that osteoblast and osteoclast cell activities are influenced by AMELX and AMBN [7], [24], [25].…”

Section: Introductionmentioning

confidence: 99%

Tracking Endogenous Amelogenin and Ameloblastin In Vivo

et al. 2014

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Research on enamel matrix proteins (EMPs) is centered on understanding their role in enamel biomineralization and their bioactivity for tissue engineering. While therapeutic application of EMPs has been widely documented, their expression and biological function in non-enamel tissues is unclear. Our first aim was to screen for amelogenin (AMELX) and ameloblastin (AMBN) gene expression in mandibular bones and soft tissues isolated from adult mice (15 weeks old). Using RT-PCR, we showed mRNA expression of AMELX and AMBN in mandibular alveolar and basal bones and, at low levels, in several soft tissues; eyes and ovaries were RNA-positive for AMELX and eyes, tongues and testicles for AMBN. Moreover, in mandibular tissues AMELX and AMBN mRNA levels varied according to two parameters: 1) ontogenic stage (decreasing with age), and 2) tissue-type (e.g. higher level in dental epithelial cells and alveolar bone when compared to basal bone and dental mesenchymal cells in 1 week old mice). In situ hybridization and immunohistodetection were performed in mandibular tissues using AMELX KO mice as controls. We identified AMELX-producing (RNA-positive) cells lining the adjacent alveolar bone and AMBN and AMELX proteins in the microenvironment surrounding EMPs-producing cells. Western blotting of proteins extracted by non-dissociative means revealed that AMELX and AMBN are not exclusive to mineralized matrix; they are present to some degree in a solubilized state in mandibular bone and presumably have some capacity to diffuse. Our data support the notion that AMELX and AMBN may function as growth factor-like molecules solubilized in the aqueous microenvironment. In jaws, they might play some role in bone physiology through autocrine/paracrine pathways, particularly during development and stress-induced remodeling.

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Enamel Matrix Derivative: A Review of Cellular EffectsIn Vitroand a Model of Molecular Arrangement and Functioning

Abstract: EMD elicits a regenerative response in periodontal tissues that is only partly replicated by amelogenin or ameloblastin components. A synergistic effect among the various proteins and with the cells, as well as a temporal effect, may prove important aspects of the EMD response in vivo.

Cited by 103 publications

References 192 publications

Novel biological activity of ameloblastin in enamel matrix derivative

Novel biological activity of ameloblastin in enamel matrix derivative

Emdogain-Regulated Gene Expression in Palatal Fibroblasts Requires TGF-βRI Kinase Signaling

Tracking Endogenous Amelogenin and Ameloblastin In Vivo

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