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Cornea Anomalies in Murine Trisomie 16
1Tost F., 2Buselmaier W., 1Wolfinger J.,
1Ernst-Moritz-Arndt-Universität Greifswald, Klinik und Poliklinik für Augenheilkunde (Greifswald)
2Universität Heidelberg, Institut für Humangenetik (Heidelberg)
Background: The prevalence rate of human Down`s syndrome is of the order 1 per 700 births. Malformations of the cornea and lens are particular clinical significance because of their outstanding importance to the optical system and function. Investigations using animal models are therefore of clinical relevance to the understanding of etiopathogenesis. As it is, no corneal changes have been reported with transgenic murine trisomy 16.
Methods: 20 fetal mice (n=40 eyes) with experimentelly induced trisomy-16 were investigated from 17th day of pregnancy in order to recognize visible developmental disorders of the cornea. All specimen were microscopically investigated in serial sections. Standardized histopathologically procedure, staining methods: Haemalaun-Eosin, Azan (Heidenhain) and PAS reaction. Evaluation with light microscopy and digital camera images system. Graduation of morphological disorders from corneal epithelium, parenchyma and endothelium (degree 1-3).
Results: In addition to disturbance of systemic development, transgenic mice fetuses exhibit malformation of the visual organ at a high level of expressivity. The cell layers and membranes of the cornea expected at the time of investigation were found in all evaluated eyes. Development and differentiation disorders of the corneal epithelial cell layers (degree 1 17,5%, degree 2 52,5%) and structural disturbances of corneal parenchyma (degree 1 2,5%, degree 2 35%, degree 3 62,5% ) were found as proof of minor corneal anomaly. Compared to normal corneal development in mice, these disturbances are interpreted as morphological indicators of a low-key corneal hypoplasia. Keratoconus is found in about 5-10% of humans suffering from Down's syndrome. Pathomorphological changes of the cornea have not been reported for murine trisomy 16. Our findings are first-ever proof of developmental disorders of the cornea in mouse fetuses with trisomy 16. These minor anomalies of the cornea could well have resulted in keratoconus in a later survival of these animals.
Conclusions: Major findings in transgenic mouse fetuses with trisomy 16 correspond with the clinical pattern of the Down's syndrome in humans. Disturbed development of lids and lens are findings of high expressivity whereas corneal hypoplasia remains at a minor intensity. Only the exact knowledge of the normogenesis makes development disturbances such as the minor anomalies of the cornea observed with murine trisomy 16 - understandable.