Abstract
Previously we identified B6.EDA+/+ mice as a novel mouse model that presents with elevated IOP and trabecular meshwork damage. Here, we expand on our previous findings by measuring aqueous humor outflow facility and analyzing the integrity of the inner wall of Schlemm's canal. As expected, intraocular pressure (IOP) was increased, and outflow facility was decreased compared to C57BL/6J controls. B6.EDA+/+ mice had significantly increased expression of the adherens junction protein, VE-cadherin by the inner wall endothelium of Schlemm's canal. These data suggest that in addition to trabecular meshwork damage, there are changes in Schlemm's canal in B6.EDA+/+ mice that lead to aqueous outflow dysfunction and ocular hypertension.
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