Surface Modifications Evoked by Estradiol and Diethylstilbestrol in Isolated Endometrial Cells: Evidence from Lectin Probes and Extracellular Release of Lysosomal Protease

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Abstract
Endometrial cells were isolated from the uteri of ovariectomized rats. The inhibitory effect of .alpha.-methyl-D-mannoside on fluorescein-labeled concanavalin A (Con A) binding to these cells indicates that they possess specific binding sites for Con A. The lectin also mediates adsorption of homologous erythrocytes to these cells. Con A binding and Con A-mediated hemadsorption to endometrial cells are depressed at 4.degree. C compared with those functions in cells maintained at 22.degree. C. Gross elevations in lectin-mediated hemadsorption to endometrial cells are evident following prior exposure to 1 .times. 10-9 M concentrations of diethylstilbestrol (DES) or estradiol-17.beta., but not to the physiologically inactive 17.alpha.-epimer, at 22.degree. C. The enhancement of hemagglutinability cannot be attributed to a corresponding increase in lectin binding at 22.degree. C. Although estrogen treatment elicited significant increments in Con A binding as early as 5 min after addition of estrogen to cell suspensions, the increment in agglutination attributable to hormone treatment consistently ranged from 1.5-3 times greater than the increase in lectin binding. These estrogenic effects were reduced by incubation of the endometrial cells at 4.degree. C or when cortisol, 3 .times. 10-6 M, was present with estradiol-17.beta.. In parallel experiments, treatment with DES and estradiol-17.beta., but not estradiol-17.alpha., also enhanced the release of cathepsin B1 and acid phosphatase from uterine segments into the particle-free extracellular media in which the tissues were incubated for 30-60 min. The marked increment in the extracellular activity of the lysosomal hydrolases induced by estrogen treatment was suppressed in cells incubated at 4.degree. C or when cortisol was present concomitantly. These and related data suggest the hypothesis that acute increments in lysosomal hydrolase activity may contribute to cell surface alterations which were malignant processes of cell growth.

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