Pietras R J, Szego C M
Endocrinology. 1975 Dec;97(6):1445-54. doi: 10.1210/endo-97-6-1445.
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. Both Con A binding and Con A-mediated hemadsorption to endometrial cells are depressed at 4 C compared with these functions in cells maintained at 22 C. Gross elevations in lectin-mediated hemadsorption to endometrial cells are evident following prior exposure to 1 X 10(-9)M concentrations of diethylstilbestrol (DES) or estradiol-17beta, but not to the physiologically inactive 17 alpha-epimer, at 22 C. The enhancement of hemagglutinability cannot be attributed to a corresponding increase in lectin binding at 22 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 C or when cortisol, 3 X 10(-6)M, was present with estradiol-17beta. In parallel experiments, treatment with DES and estradiol-17beta, but not estradiol-17 alpha, also enhanced the release of cathepsin B 1 and acid phosphatase from uterine segments into the particle-free extracellular media in which the tissues had been 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 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 have been described in both normal and aberrant processes of cell growth.
从去卵巢大鼠的子宫中分离出子宫内膜细胞。α-甲基-D-甘露糖苷对荧光素标记的伴刀豆球蛋白A（Con A）与这些细胞结合的抑制作用表明，它们具有Con A的特异性结合位点。凝集素还介导同源红细胞吸附到这些细胞上。与在22℃下维持的细胞相比，在4℃时Con A与子宫内膜细胞的结合以及Con A介导的血细胞吸附均受到抑制。在22℃下，预先暴露于1×10⁻⁹M浓度的己烯雌酚（DES）或雌二醇-17β后，凝集素介导的子宫内膜血细胞吸附明显升高，但对生理上无活性的17α-差向异构体则无此现象。在22℃下，血凝性的增强不能归因于凝集素结合的相应增加。尽管雌激素处理在向细胞悬液中添加雌激素后最早5分钟就引起Con A结合的显著增加，但激素处理引起的凝集增加始终比凝集素结合的增加大1.5至3倍。在4℃下孵育子宫内膜细胞或当存在3×10⁻⁶M的皮质醇与雌二醇-17β时，这些雌激素作用会减弱。在平行实验中，用DES和雌二醇-17β处理，但不用雌二醇-17α处理，也增强了组织在其中孵育30至60分钟的子宫段组织中组织蛋白酶B1和酸性磷酸酶释放到无颗粒细胞外培养基中的量。雌激素处理诱导的溶酶体水解酶细胞外活性的显著增加在4℃下孵育的细胞中或同时存在皮质醇时受到抑制。这些及相关数据提出了一个假设，即溶酶体水解酶活性的急性增加可能导致细胞表面改变，这在细胞生长的正常和异常过程中均有描述。
