Purchase this article with an account.
A. R. Wegener, S. Günther; Disturbances of Lens Epithelial Growth Control in the APO E Mouse Model. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2796. doi: https://doi.org/.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To investigate the mechanisms of epithelial malformation in the lenses of the APO E deficient mouse. Anterior polar cataracts were found in close to 100% of all APO E mouse lenses in a one year study. Degenerative defects of the corneal epithelium occurred at a similar frequency. Nutritional effects could be ruled out, because none of the abnormalities observed showed any correlation to the different diets, the animals were exposed to.
APO E deficient mice from a one year study, performed under SPF standard conditions, were sacrificed at the 3, 6, 9 and 12 months interval (10 animals/time point) and their eyes were fixated in para-formaldehyde and processed for light microscopic investigations. In addition to haematoxilin eosin staining antibodies against smooth muscle actin, vimentin, FGF and endoglin were used.
Lens epithelial degenerations, partly with thinning of the overlaying capsule, but also hyperplasia of the central epithelium, disturbances of the nuclear bow region, swelling and liquefaction of superficial cortical fibre cells and globular degeneration in the posterior sub-capsular region (PSC) were quite frequent. The posterior capsule of the lens demonstrated a marked thinning during PSC formation leading in some cases to capsular rupture and formation of a posterior lens coloboma. The largest number of pathological changes was found at the 6 and 12 months intervals, but epithelial hyperplasia occurred already at the 3 months interval. Vimentin and FGF staining pointed at marked disturbances of epithelial growth and fibre cell differentiation control.
The high frequency of epithelial hyperplasia and the unusual staining for vimentin and FGF point at an isolated disturbance of lens epithelial growth control leading to the formation of anterior polar cataracts in the APO E mouse. In spite of frequent fibre swelling and degeneration in the lens bow region, there were only few cortical cataracts and in most of the lenses the cortex and nucleus remained transparent. The pathological changes observed cannot be regarded as ageing changes alone.
This PDF is available to Subscribers Only