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H. P. Solari, G. A. Novais, G. Lima, D. Cheema, R. N. Belfort, M. N. Burnier, Jr.; Immunohistochemical Expression of Lysyl Oxidase in Keratoconus. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4545.
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Lysyl Oxidase (LOX) is an extracellular amine oxidase that plays a critical role in the biogenesis of connective tissue matrices by crosslinking the extracellular matrix proteins collagen and elastin. The expression of LOX in the ocular tissues remains unknown. Keratoconus is a bilateral asymmetric corneal ectasia. The most important histopathological features of Kerataconus include stromal defects such as breaks in Bowman’s layer. Recently, epithelial thinning was reported as a prominent feature in this particular disease. The purpose of this study was to compare the expression of LOX in the different layers of normal and Kerataconus corneas.
Formalin-fixed, paraffin-embedded sections of 6 keratoconus patients who underwent penetrating keratoplasty and 2 normal control corneas from cadavers were stained with Hematoxylin and Eosin (H&E) for histopathological assessment. Immunohistochemistry using an antibody against Lysyl Oxidase was performed using the Ventana BenchMark fully automated machine. The slides were analysed at the Henry C. Witelson Ocular Pathology Laboratory and the samples were evaluated for positivity in the corneal epithelium, Bownman’s layer, corneal stroma, Descemets membrane and endothelium.
The corneal epithelium and endothelium were positive for LOX in 100% of patients with Keratoconus. In the control corneas, the endothelium stained positive and the epithelium was negative for LOX in all samples. The stroma, Bownman’s layer and Descemet membrane did not show significant positivity in either of the groups in this study.
The positive expression of LOX in the epithelium of all Keratoconus corneas supports the recent finding of corneal epithelium involvement in this disease. Moreover, the lack of stromal staining in either Keratoconus or normal corneas, in addition to the absence of LOX staining in the epithelium of normal corneas, suggests that the epithelium plays an important role in the pathogeneses of this disease. It is possible that LOX is upregulated as a compensatory mechanism in advanced stages of the disease.
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