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We have previously shown that gap junctions and gap junction-associated protein connexin 43 are present in the human and baboon corpus luteum. Abundant expression of connexin 43 is seen in the midluteal phase corpora lutea. Since the formation of gap junctions requires the presence of adherens junctions formed by the cadherins, our aim in these studies was 1) to immunocytochemically localize E-cadherin and the associated proteins, beta-catenin and gamma-catenin (plakoglobin), in the baboon corpus luteum; 2) to determine by Western analysis the levels of these proteins in early, mid-, and late luteal phase and atretic baboon corpora lutea; and 3) to examine whether or not cell-cell contact in cells in culture is disrupted by the addition of the antibody for E-cadherin. E-cadherin was localized to the peripheral cell membranes of luteal cells at all stages examined, except atretic corpora lutea, with the strongest immunoreactivity in the early luteal phase. Both beta-catenin and plakoglobin were localized in the cytoplasm of the luteal cells. Immunoreactivity for all three peptides was not observed in nonluteal tissue. By Western analysis, abundant expression of E-cadherin was observed in the early luteal phase, and the level of expression was significantly different from that observed in the mid- and late luteal phase corpora lutea. In contrast, the levels of beta-catenin and plakoglobin were higher in the midluteal phase compared to the early luteal phase. Addition of the E-cadherin antibody to early luteal phase cells in culture disrupted the cell-cell contacts between cells. Thus, cell adhesion involving E-cadherin may play a significant role in the cyclic development and demise of this tissue.

Prostaglandins (PGs) are thought to have an important function in the initiation and/or propagation of parturition. To define the relationship of individual PGs to one another and compare their alterations with gestational age, PGF, PGE, 6-keto-PGF1 alpha (6KF) and thromboxane B2 (TxB2) were measured in uterine and placental tissue and uterine venous plasma of rats at Days 15, 18, 19, 20, and 21 of pregnancy and at delivery (Day 21 1/2). In addition, concomitant measurements of peripheral plasma estradiol (E2), estrone (E1) and progesterone (P) and pituitary oxytocin (OT) content, putative regulators and/or modulators of PG metabolism, were determined. Significant enhancements (P less than 0.05) in uterine 6KF, TxB2, PGF and PGE concentrations (ng/mg DNA) were detected by Day 20 compared to Day 15 of pregnancy and further dramatic increases were found on Day 21 and at delivery. Although uterine 6KF was present in the highest concentrations, PGF showed the greatest increment from Day 15 to delivery. No alterations in uterine venous plasma PGE or PGF concentration were found with gestational age but 6KF and TxB2 showed significant increases at delivery. The placental concentrations of PGs were approximately 1/50 of uterine tissue. Placental PGE and PGF concentrations (ng/mg DNA) increased only slightly at delivery but the augmentation in 6KF and TxB2 levels were of greater magnitude. Significant increases in E2 and E1 with reciprocal decreases in P occurred on Day 21 of pregnancy. In contrast, pituitary OT content showed no alterations at any of the days examined. These results are consonant with the hypothesis that uterine PGs have an important function in parturition and uterine-placental physiology, and suggest that an increasing estrogen/P ratio at the end of pregnancy is related to enhanced uterine PG levels.