+49 30 838 53555
Placental growth can be achieved by either cellular proliferation or hypertrophy. Tissue regeneration and the nutrition of the fetus via embryotrophe require high rates of cellular turnover and the so-called pre-term 'maturation' of the placenta is correlated with a reduction of maternal crypt epithelial cells. Placentomes of 45 pregnant cows were collected from an abattoir to assess the role of proliferation and apoptosis in placental physiology and pathology. Placentomes were also taken from five cows undergoing premature Caesarean section and from ten naturally calving cows immediately after the expulsion of the fetus. Five of these animals had not released the fetal membranes after 12 h. Tissue sections of placentome were assessed for the Ki-67 protein; the TUNEL procedure was performed and verified by transmission electron microscopy. The maternal crypt epithelium and the fetal chorionic epithelium had a higher percentage of Ki-67-positive cells than the stroma. The percentage of Ki-67-positive cells increased significantly during pregnancy in fetal chorionic epithelium and was significantly decreased in fetal chorionic epithelium and maternal crypt epithelium after the expulsion of the fetus in comparison with tissue from month 9 of pregnancy. The number of apoptotic cells increased significantly during pregnancy in maternal crypt epithelium, maternal stroma and fetal chorionic epithelium as detected in slaughtered animals. Significantly more apoptotic fetal chorionic epithelial cells were found in animals retaining their fetal membranes in comparison with prepartum cattle during month 9 of pregnancy, at premature section and in animals releasing the fetal membranes completely. The results strongly indicate that bovine placentomes have cell type-specific rates of cellular turnover reflecting tissue growth, embryotrophe and placental maturation. Retention of fetal membranes is characterized by a large number of fetal chorionic epithelial cells undergoing apoptosis immediately after the expulsion of the fetus. This finding indicates that incomplete maturation of placentomes plays an important role in fetal membrane retention and that massive apoptosis after the expulsion of the fetus should be the consequence of diminished blood supply to the uterus, as verified in a recent study.