Calbindin-Dgk was quantified and its cellular location was defined in uterus, yolk sac, and placenta. In late gestation (days 17 to term) coordinated induction of calbindinDqk was seen in uterine epithelial lining cells and the juxtaposed yolk sac visceral epithelium as well as the intraplacental yolk sac epithelium. The induction of calbindin-Dk in these cells coincided with the time of exponential fetal bone growth and maximal fetal accumulation of calcium, suggesting a role of the protein in these epithelial layers in maternal-fetal calcium transport. Dynamic changes also occurred in the calbindin-Dgk contents of the two layers of uterine smooth muscle (outer longitudinal and inner circular) during mid-and late gestation.
Radioimmunoassay (RIA) data on concentrations of circulating steroids in normal prepubertal and adult male and female humans, chimpanzees, rhesus monkeys, rats, mice, and hamsters have been collated from the literature. Few reports include data for both sexes, for age groups, or for more than one species. In selecting references for inclusion in the tables, efforts were made to choose data only from RIA procedures that were adequately validated. A number of similarities can be found by reviewing the tables. Levels of estradiol appear somewhat similar for humans, chimpanzees, and rhesus monkeys of both sexes. Among the notable differences are the levels of estradiol and progesterone in primates and rodents, the apparently high level of aldosterone in mice, and the patterns of progesterone secretion in mice and rats. All values in the tables have been converted to picograms for easy comparison between steroids and species. Data for humans are fairly complete, but there is a significant lack of information for several other species.
The present studies were undertaken to characterize the expression of calcium binding protein (CaBP or calbindin-D9k) in uterine tissues. Using immunohistochemical techniques, calbindin-D9k was localized to the uterine (luminal) epithelium of pregnant rats, but not present in the uterine epithelium of nonpregnant rats. Calbindin was found also in the uterine smooth muscle and endometrial stromal cells of pregnant animals. These latter localizations were reproduced in uteri of 21-day-old nonpregnant rats by administration of tamoxifen or physiological doses of estrogens. Estrogen and tamoxifen produced half-maximal increases of uterine calbindin at daily doses of 0.1 and 10 micrograms, respectively, and maximal responses at 0.3 and 40 micrograms/day. Testosterone and progesterone, at doses which increased the growth of the uterus, did not induce calbindin-D, and both hormones blocked estradiol's effect on uterine calbindin-D appearance. The epithelial localization of calbindin in pregnant uteri was not reproduced in nonpregnant animals by either estradiol (3 micrograms/day) or progesterone (1 mg/day). The localization of calbindin in uterine epithelium during pregnancy appears to be dependent upon an as yet unknown factor. In view of the large surface area of the luminal epithelium in pregnant animals, and the pregnancy-related expression of calbindin in these cells, we propose that uterine epithelium plays an important role in transport of calcium during pregnancy.
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