Proliferation and apoptosis in bovine placentomes during pregnancy and around induced and spontaneous parturition as well as in cows retaining the fetal membranes

Abstract

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.

Histo-morphology of the Uterus and Early Placenta of the African Buffalo (Syncerus caffer) and Comparative Placentome Morphology of the African Buffalo and Cattle (Bos taurus)

“…Uterine samples of cattle (B. taurus) (n = 12) were collected during an earlier study by Boos et al [13].…”

“…HE-slides of placentomal tissue from Holstein Friesian cows were obtained from the Anatomical Institute of the Vetsuisse Faculty of Zurich, Switzerland [13]. Cattle samples were investigated by LM only.…”

Apoptose e maturação placentária bovina: um estudo imunohistoquímico e morfométrico

“…Proteínas como Bax e Bid são pró-apoptóticas e ativam caspases efetoras (Patel & Gores 1998). A maturação placentária é mediada pela apoptose das células das criptas do epitélio materno e ocorre durante toda a gestação na renovação normal (Boos et al 2003), aumentando no terço final. Straszewski-Chavez et al (2005) avaliaram placentas humanas e demonstraram maior apoptose nos sítios de invasão do trofoblasto no epitélio materno, sugerindo que este processo facilite a invasão do trofoblasto e a remodelação dos vilos endometriais.…”

The role of placental MHC class I expression in immune-assisted separation of the fetal membranes in cattle

“…The loss of fetalmaternal adherence in cattle is believed to involve several processes: i) Collapse of the fetal-placental circulation, leading to shrinking of the placentomal villi (Laven and Peters, 1996) ii) Placental-maturation, characterized by a decrease in the number and the height of maternal epithelial cells (Boos et al, 2003;Laven and Peters, 1996) and a drop in BNC numbers (Gross et al, 1991;Williams et al, 1987) iii) Breakdown of the extracellular matrix linking the fetal and maternal epithelium (Beagley et al, 2010). The first indications for the involvement of the maternal immune system in the loss of fetal-maternal adherence and the occurrence of RFM were provided by Gunnink (Gunnink, 1984a;Gunnink, 1984b).…”

“…IL-1β, IL-6, TNF-α) (Chazaud, 2014). In cattle the mRNA expression levels of the pro-inflammatory cytokines IL-1β, IL-6 Placental maturation is characterized by increased apoptosis of trophoblasts and maternal endothelium (Boos et al, 2003) and is one of the processes believed to be involved in the loss of fetal-maternal adherence (Boos et al, 2003;Laven and Peters, 1996). Uterine macrophages produce TNF-α (Davies et al, 2004), which can induce apoptosis in cells and as such may influence placental maturation.…”