Placental hormones and fetal-placental development

Abstract

Production of growth promoting substances by the placenta is regulated differently from the way production of similar compounds is regulated by maternal organs in various cases. Gene duplication is one of the mechanisms that facilitated the evolution of placental specific endocrine activity. Cattle, sheep and goats, although evolutionarily related, differ significantly from each other in the way their placental growth hormone (GH) and prolactin (PRL)-like hormones have evolved. Cattle carry one copy of the GH gene and there is no evidence yet for expression of that single GH gene copy in the placenta. On the other hand, the ovine GH gene has been duplicated and both oGH copies are expressed in the placenta during early stages of gestation. Prolactin gene duplication in ruminants resulted in the formation of specific placental-expressed prolactin-related genes including the placental lactogen (PL) gene. In homologous state, ovine PL manifests PRL activity, but antagonizes GH activity. Ovine PL activity which can be mediated by PRL receptors or by hetero-dimerization of GH and PRL receptors, provide a novel regulatory mechanism for somatogenic activity dependent on the coexistence of both GH and PRL receptors in the same cells. Another mechanism for specific placental endocrine activity is silencing of the alleles through genetic imprinting. Disruption of genetic imprinting of placental genes has been proposed as one of the explanations for the loss of cloned fetuses generated by somatic cell nuclear transfer.