Purpose: To evaluate whether selective laser trabeculoplasty and prostaglandin analogs regulate the permeability of cultured human Schlemm canal cells by inducing intercellular junction disassembly. Design: Laboratory investigation. Methods: Intercellular junctions were made visible in living cells by making them fluoresce after transfection with a plasmid expressing the zonula occludens 1 protein tagged with green fluorescent protein. Schlemm canal cells were treated by direct laser irradiation; by exposure to media conditioned by either lasered Schlemm canal cells or trabecular meshwork cells; by exposure to the prostaglandin analogs latanoprost, bimatoprost, and travoprost; or by the addition of the nonprostaglandin agents brimonidine, timolol, and dorzolamide. Junction disassembly was monitored using fluorescence microscopy, and permeability alterations were measured as changes in conductivity using flow meters. Results: The direct laser irradiation of Schlemm canal cells caused a 3-fold increase in conductivity. Exposure of the cells to media conditioned by lasered Schlemm canal cells or trabecular meshwork cells induced junction disassembly and a 2- to 4-fold increase in conductivity. Exposure to prostaglandin analogs also induced junction disassembly and a 4- to 16-fold increase in conductivity, whereas the 3 nonprostaglandin agents tested were ineffective in both regards. Conclusions: Exposure to factors secreted by lasered Schlemm canal cells and lasered trabecular meshwork cells and the application of prostaglandin analogs induced junction disassembly while increasing the permeability of Schlemm canal cells. These findings support our hypothesis that selective laser trabeculoplasty and prostaglandin analogs share a common mechanism that likely mediates their pressure-lowering effects.
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