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Amelogenin:: A Potential Regulator of Cementum-Associated Genes

  • Autores: Hema L. Viswanathan, Janice E. Berry, B. L. Foster, Carolyn W. Gibson, Yong Li, A. B. Kulkarni, Malcolm L. Snead, Martha J. Somerman
  • Localización: Journal of periodontology, ISSN 0022-3492, Vol. 74, Nº. 10, 2003, págs. 1423-1431
  • Idioma: inglés
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  • Resumen
    • Background: Studies suggest that enamel matrix proteins induce differentiation and mineralization of a variety of mesenchymal cells, including odontoblasts, osteoblasts, and cementoblasts. It has been postulated that this activity could be due to amelogenin-like proteins, known to be present in some mixtures of enamel matrix derivatives. Amelogenins have been reported to induce expression of a mineralized tissue-specific marker, bone sialoprotein (BSP), indicating that epithelial products can regulate the activity of mesenchyme-derived cells.

      Methods: To explore the molecular mechanisms involved in BSP regulation, a clonal population of immortalized murine cementoblasts (OCCM-30) was exposed to full-length murine amelogenin protein (rp(H)M180), 0.1 µg/ml to 10.0 µg/ml, for 8 days in vitro. To further investigate the potential epithelial-mesenchymal interaction, an amelogenin knockout mouse model was used to examine expression of BSP and other markers, including Type I collagen, in tissue samples.

      Results: The lowest dose of amelogenin slightly enhanced BSP expression, whereas at the highest dose, a dramatic decrease (three-fold) in BSP expression was observed. Parallel experiments showed a corresponding decrease in mineral nodule formation in vitro for cells treated with the higher dose of rp(H)M180. In situ hybridization and immunohistochemical analysis of sections from amelogenin null mice revealed a dramatic reduction in expression of BSP mRNA and protein in cementoblasts and surrounding osteoblasts in comparison to age-matched controls. In contrast, the expression of Type I collagen was not significantly different from controls.

      Conclusion: These data suggest that amelogenin may be a critical signaling molecule required for appropriate development of the periodontium. J Periodontol 2003;74:1423-1431.


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