Fetal growth restriction in hypothyroidism is associated with changes in proliferative activity, apoptosis and vascularisation of the placenta

Abstract

The objective of this study was to evaluate fetal weight, histomorphometric changes and proliferative activity, apoptosis and angiogenesis of the placenta in rats with hypothyroidism. Thirty-six adult female rats were divided into two groups with 18 animals each: control and hypothyroidism. Hypothyroidism was induced by daily administration of propylthiouracil (1 mg/animal). The administration began five days before becoming pregnant and the animals were sacrificed at 14 or 19 days of gestation. The control group received a placebo. The number and weight of fetuses and the rate of fetal death was determined, as well as the morphometric characteristics, the immunohistochemical expression of cell division control protein 47 (CDC)-47 and vascular endothelial growth factor (VEGF) and the number of apoptotic cells in the placental disk. The data were analysed by Mann–Whitney U test. Hypothyroidism reduced the weight of fetuses and of the uterus and placenta (P < 0.05), altered the thickness of the placental labyrinth and spongiotrophoblast (P < 0.05), increased the population of glycogen cells in the spongiotrophoblast (P < 0.05), interfered with the vascular development of the placental labyrinth and decreased VEGF expression (P < 0.05), reduced the expression of CDC-47 and cellularity and increased the apoptotic rate in the placental disk (P < 0.05). We conclude that hypothyroidism affects fetal weight by altering the proliferative activity, apoptosis and vascularisation of the placenta.