Disease relevance of Ameloblasts

• We examined whether heterotrimeric G proteins participated in the disruption of vesicular trafficking of the secretory ameloblast exposed to fluoride, using immunoblotting and pertussis toxin (IAP)-induced adenosyl diphosphate (ADP)-ribosylation for membrane fractions of the cell [1].
• This staining was markedly reduced in ameloblasts of rats given either 10 or 20 mg sodium fluoride per kg body weight [2].

High impact information on Ameloblasts

• During the late bell stage, TGF beta 2 gene expression shifted from the mesenchyme to the odontogenic epithelium and was colocalized with protein, suggesting an autocrine role for the terminal differentiation of ameloblasts [3].
• Ameloblastin, an enamel matrix protein, is expressed by differentiating ameloblasts [4].
• Expression of Notch 1, 2 and 3 is regulated by epithelial-mesenchymal interactions and retinoic acid in the developing mouse tooth and associated with determination of ameloblast cell fate [5].
• However, Shh signaling is not essential for differentiation of ameloblasts or odontoblasts [6].
• Unlike that observed in osteoblast differentiation, Cbfa1 is downregulated in fully differentiated odontoblasts and is surprisingly expressed in ectodermally derived ameloblasts during the maturation phase of enamel formation [7].

Biological context of Ameloblasts

• Ameloblastin is a cell adhesion molecule required for maintaining the differentiation state of ameloblasts [4].
• We postulate that the epithelial cells of the root sheath as well as the ameloblasts are synthesizing amelin which might be one of the key proteins coupled to the process of cementogenesis [8].
• We conclude that EMSP1 is expressed by pig and mouse ameloblasts during the early maturation stage of amelogenesis [9].
• Laminin gamma2 expression is developmentally regulated during murine tooth morphogenesis and is intense in ameloblasts [10].
• Alternative splicing of amelogenin mRNA from rat incisor ameloblasts [11].

Anatomical context of Ameloblasts

• At the bell stage of tooth development, Hox-8 expression switches tissue layers, being absent from the differentiating epithelial ameloblasts and turned on in the differentiating mesenchymal odontoblasts [12].
• It is now known that DMP1 is not unique to dentin but is present in other mineralized tissues like long bone, calvaria, and ameloblasts [13].
• E-cadherin was distributed in proliferating cells of the inner and outer enamel epithelia but not in differentiated cells such as ameloblasts, whereas N-cadherin expression was up-regulated in differentiated epithelial cells [14].
• Because ameloblasts are responsible for dental enamel formation, we used an ameloblast-derived cell line (LS8) to characterize specific responses to fluoride treatment [15].
• In situ hybridization of mandibles of 1-day-old mice detected TIP39 RNA in secretory ameloblasts and odontoblasts [16].

Associations of Ameloblasts with chemical compounds

• To determine the efficiency of antisense treatment in this model system, digoxigenin-labeled oligodeoxynucleotides were observed to diffuse throughout the tooth explants including the target ameloblast cells within 24 hours [17].
• Tetracycline was administered to rats in varying doses in order to study the likelihood of ultrastructural alterations to ameloblasts and to study odontoblasts and dentin as well [18].
• The parent protein is a 186-kDa glycoprotein that concentrates along the secretory face of the ameloblast Tomes' process [19].
• Maturing enamel overlaid by either ruffle-ended or smooth-ended maturation ameloblasts showed similar Ca and P concentrations [20].
• The visualization of the patterns of ameloblast modulation by the glyoxal bis(2-hydroxyanil) staining method [21].

Gene context of Ameloblasts

• The GMp motif in the N-terminal region of the cytokeratin 14 of ameloblasts binds to trityrosyl motif peptide (ATMP) of amelogenin (Ravindranath, R. M. H., Tam, W., Bringas, P., Santos, V., and Fincham, A. G. (2001) J. Biol. Chem. 276, 36586 - 36597) [22].
• Amelogenin interacts with cytokeratin-5 in ameloblasts during enamel growth [22].
• In early secretory ameloblasts, DSPP expression was transient and down-regulated with the appearance ofdentin matrix [23].
• In situ hybridization studies showed expression of Dmp1 in odontoblasts with transient expression in secretory ameloblasts [24].
• Quantitative analyses identified specific modulations of Dlx-2 expression in ameloblasts depending on the anatomical sites of the incisor, showing more specifically an inverse linear relationship between the Dlx-2 promoter activity level and enamel thickness [25].

Analytical, diagnostic and therapeutic context of Ameloblasts

• Immunofluorescence revealed that disorganization of the ameloblast layer was associated with a loss of laminin-5, an extracellular matrix molecule mediating epithelial anchorage [26].
• Amelogenin amplification products were detected only in the secretory ameloblast layer after 20 cycles of PCR [27].
• Northern blot and in situ hybridization analysis performed for five putative novel genes and one new isoform of amelogenin revealed differential expression levels in the osteoblasts, ameloblasts and the odontoblasts of the developing rat molars [28].
• Immunohistochemical and Western blot analyses with an affinity-purified antipeptide antibody specific for the enamelin carboxyl terminus demonstrate that enamelin is synthesized and secreted by secretory-phase ameloblasts [19].
• In immunocytochemistry, CBP was localized in ameloblast nuclei in the maturation zone but not in the secretion and transition zones [29].

References