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E.L. Macnamara, W.G. Sams, K. Smith, J. Ambati, N. Singh, B. Ambati; Aquaporin–1 Expression is Decreased in Human and Mouse Corneal Endothelial Dysfunction . Invest. Ophthalmol. Vis. Sci. 2004;45(13):4795.
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Purpose: To determine if aquaporin–1, a water channel involved in fluid transport, expression is decreased in human and mouse corneal endothelial dysfunction. Methods:Immunohistochemistry with anti–aquaporin 1 antibody and confocal microscopy were used to study a case series of human corneal specimens, and a mouse model of corneal endothelial injury was created with injection of 0.01% benzalkonium chloride into the anterior chamber with a 33gauge needle. Western blotting was used to provide confirmatory evidence. Results:Specimens from 18 consecutive patients undergoing corneal transplantation were performed. Of these, 10 had endothelial dysfunction (4 – Fuchs’ dystrophy, 5 –bullous keratopathy, 1 – corneal graft failure). Two had keratoconus and 6 had corneal scarring from trauma or infection. Three normal central corneal specimens from donor tissue harvested for limbal stem cell transplantation were also examined. Aquaporin–1 was found to be expressed primarily in the endothelium in normal human cornea. In human corneas with endothelial disease, aquaporin–1 expression was decreased in corneal endothelium but upregulated in the posterior stroma. In human corneas with non–endothelial corneal disease, aquaporin–1 expression resembled the normal pattern. This was confirmed on Western blotting. Normal mice demonstrate aquaporin–1 expression both in the endothelium and the stroma. In mouse corneas subjected to corneal endothelial injury, aquaporin–1 was reduced in the endothelium but upregulated in the posterior stroma. Conclusions: Corneal endothelial injury is associated with decreased aquaporin–1 expression in the endothelium but upregulation in the posterior stroma.
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