The acid phosphatase alkaline phosphatase lactate dehydrogenase and succinate dehydrogenase in the endothelium on the trabecular meshwork in primary glaucoma were studied.
Results cultured cells showed the specific characteristics of bovine trabecular meshwork cells.
Changes in the microstructure of the trabecular meshwork may cause a decrease in outflow facility and an increase in IOP.
Conclusion Human trabecular meshwork cells can be successfully cultured in vitro.
Conclusion The expression of AQP-1 is inhibited by Dex in bovine trabecular meshwork cells. It may be one of reasons that retard the aqueous outflow in corticosteroid induced glaucoma.
The mechanism of elevated intraocular pressure is increased aqueous outflow resistance owing to an accumulation of extracellular matrix material in the trabecular meshwork.
Effect of chloride channel inhibitor on human trabecular meshwork cells
Effects of tumor necrosis factor-α on fibronectin of cultured bovine trabecular meshwork cells in vitro
Expression of messenger RNA for transforming growth factor β 1 in bovine trabecular meshwork
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