Evidence for regulation of amelogenin gene expression by 1,25-dihydroxyvitamin D3 in vivo

✍ Scribed by Petros Papagerakis; Dominique Hotton; Frederic Lezot; Steve Brookes; William Bonass; Colin Robinson; Nadine Forest; Ariane Berdal

• Publisher: John Wiley and Sons
• Year: 2000
• Tongue: English
• Weight: 437 KB
• Volume: 76
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/(sici)1097-4644(20000201)76:2<194::aid-jcb4>3.0.co;2-u

✦ Synopsis

The unique hereditary enamel defect clearly related to the disturbance of one enamel matrix protein is X-linked amelogenesis imperfecta (AI), in which several mutations of amelogenin gene have been identified. The clinical phenotype of many of these subjects shows similarities with enamel defects related to rickets. Therefore, we hypothesized that rachitic dental dysplasia is related to disturbances in the amelogenin pathway. In order to test this hypothesis, combined qualitative and quantitative studies in experimental vitamin D-deficient (ϪD) rat model systems were performed. First, Western blot analysis of microdissected enamel matrix (secretion and maturation stages) showed no clear evidence of dysregulation of amelogenin protein processing in ϪD rats as compared with the controls. Second, the ultrastructural investigation permitted identification of the internal tissular defect of rachitic enamel, the irregular absence of intraprismatic enamel observed in ϪD animals, suggesting a possible link between prism morphogenesis and vitamin D. In addition, the steady-state levels of amelogenin mRNAs measured in microdissected dental cells was decreased in ϪD rats and up-regulated by an unique injection of 1,25-dihydroxyvitamin D 3 (1,25(OH) 2 D 3 ). The present study shows evidences that amelogenin expression is regulated by vitamin D. This is the first study of an hormonal regulation of tooth-specific genes.