Detection of glucocorticoid receptors in cultured human trabecular cells.

To evaluate potential direct effects of glucocorticoids on the aqueous outflow pathway, the cellular binding of steroids to cultured human trabecular cells was examined. After incubation of cells with 5 to 40 nM [3H]dexamethasone, specific binding (i.e., binding that could be blocked by an excess of nonlabeled steroid) was detected by measuring the total cell-associated labeled hormone. A binding affinity of 5 nM and 60,000 receptor sites/cell were demonstrated with labeled dexamethasone. Incubation of human trabecular cells with 40 nM [3H]dexamethasone for 60 min revealed that 62% +/- 7 of the specific binding was found in the nuclear fraction and 38% +/- 3 was in the cytoplasmic fraction. In competition studies, dexamethasone had a higher affinity for these sites than cortisol, which in turn had a higher affinity than progesterone. These studies suggest that functional glucocorticoid receptors are present in human trabecular cell cultures. Therefore it is possible that a direct action of glucocorticoids on trabecular cells could contribute to the decreased outflow facility observed in steroid glaucoma.