Assessment of amelogenin expression in follistatin overexpressing mice
Journal Title: Journal of Stomatology (Czasopismo Stomatologiczne) - Year 2013, Vol 66, Issue 4
Abstract
Introduction. Amelogenesis takes place under the control of numerous morphogenetic proteins. Disturbances in their secretion may manifest themselves in several developmental pathologies of this tissue. At the same time, disorders in specific proteins may cause deregulation of expression of other regulatory or structural particles. Aim of the study. To compare expression of amelogenin in transgenic mice with follistatin overexpression and in standard mice. Material and method. The material comprised tooth germs of maxillary first molar dissected on day 10 and on day 19 of the fetal life of transgenic and standard mice. The mRNA expression of the gene responsible for synthesis of amelogenesis was assessed based on polymerase chain reaction (PCR) preceded by the process of reverse transcription, i.e. transcription of single-stranded matrix ribonucleic acid into double-stranded DNA. Results. On day 10 of mice fetal life two types of amelogenin mRNA were discovered. The mRNA concentrations in specific products of amelogenin transcription (A1 and A2) in the material obtained from gene-modified animals were statistically significantly lower than in standard animals. Medians of mRNA concentrations of the amelogenin second splicing variant were significantly higher than in the material obtained from the first (A1), both in standard and transgenic mice. Analysis performed on day 19 of genetycznefetal life did not show any presence of amelogenin in the enamel organ. Conclusion. Genetic modification resulting in follistatin overexpression in epithelium significantly lowered the activity of the gene responsible for amelogenin synthesis, and may explain developmental defects of enamel in transgenic mice. Different expression of amelogenin splicing variants indicates that a mouse with built-in follistatin gene could be a valuable animal model useful in studies on amelogenesis imperfecta.
Authors and Affiliations
Jarosław Gibek, Elżbieta Pawłowska, Joanna Szczepańska
Keywords
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