Prl7b1, also known as prolactin-like protein-N (PLP-N), is a member of the prolactin (PRL) family of hormones and cytokines. It is involved in pathways regulating placental adaptations to physiological stressors, and may play a role in the development of the uterine endometrium [1,4]. Genetic models, such as knockout (KO) mouse models, are valuable tools for studying its functions.

In a Prl7b1 KO mouse model, homozygous mutant mice were viable and fertile. Under standard housing conditions, Prl7b1 had no detectable impact on placentation and pregnancy. However, during pregnancy with hypoxia exposure, wild-type placentas showed adaptations that were absent in Prl7b1 null placentation sites, indicating Prl7b1's role in placental responses to physiological stressors [1]. Disruption of Prl7b1 in rats did not adversely affect placental development, and the Prl7b1 locus could be used to drive Cre recombinase expression in invasive trophoblast cells, which may help investigate genes regulating these cells [2,3]. In neonatal mouse uterine development, Prl7b1 expression increased significantly on Postnatal day 9, suggesting its involvement in endometrial adenogenesis [4]. Maternal oxycodone treatment in mice led to up-regulation of Prl7b1 in female placentas, along with histological changes, indicating its response to drug-induced placental pathophysiology [5].

In conclusion, Prl7b1 is mainly associated with placental adaptations to stress, uterine endometrial development, and placental responses to drug-induced pathophysiology. Studies using Prl7b1 KO mouse and conditional mutant rat models have provided insights into its role in these biological processes, which may contribute to understanding related pregnancy-associated conditions and uterine development-related diseases.