Prl7b1, also called PRL-like protein-N (PLP-N), is a member of the prolactin (PRL) family. The PRL family participates in regulating optimal reproductive performance. Prl7b1 is likely part of a pathway regulating placental adaptations to physiological stressors [1]. Gene knockout (KO) mouse models have been crucial for studying its function.

In a Prl7b1 KO mouse model, homozygous mutant mice were viable and fertile, and under standard conditions, Prl7b1 had no detectable effects on placentation and pregnancy. However, when pregnant mice were exposed to hypoxia, wild-type placentas showed adaptations that were absent in Prl7b1 null placentation sites, indicating its role in placental response to stress [1]. In rats, although disruption of Prl7b1 did not affect placental development, the Prl7b1 locus can drive Cre recombinase expression in invasive trophoblast cells, providing a new conditional knockout (CKO) model for studying genes regulating invasive trophoblast cells and uterine spiral artery remodeling [2,3]. In neonatal mice, Prl7b1 expression suddenly increased significantly on Postnatal day 9 during endometrial adenogenesis [4]. In the mouse placenta, maternal oxycodone treatment led to up-regulation of Prl7b1 in female placentas, along with histological changes [5]. In the murine placenta, Prl7b1 is a marker gene for the junctional zone [6].

In conclusion, Prl7b1 is mainly involved in placental adaptations to physiological stressors, and its role in placental development and response to stress has been revealed through KO and CKO mouse models. Its expression changes also occur during endometrial adenogenesis in neonatal mice and in response to maternal oxycodone treatment in the placenta. These findings contribute to understanding placental-related processes and potentially related diseases.

References:

1. Bu, Pengli, Alam, Sheikh M Khorshed, Dhakal, Pramod, Vivian, Jay L, Soares, Michael J. 2016. A Prolactin Family Paralog Regulates Placental Adaptations to a Physiological Stressor. In Biology of reproduction, 94, 107. doi:10.1095/biolreprod.115.138032. https://pubmed.ncbi.nlm.nih.gov/26985002/

2. Iqbal, Khursheed, Nixon, Brandon, Crnkovich, Benjamin, Vivian, Jay L, Soares, Michael J. 2023. CONDITIONALLY MUTANT ANIMAL MODEL FOR INVESTIGATING THE INVASIVE TROPHOBLAST CELL LINEAGE. In bioRxiv : the preprint server for biology, , . doi:10.1101/2023.08.02.551740. https://pubmed.ncbi.nlm.nih.gov/37577576/

3. Iqbal, Khursheed, Dominguez, Esteban M, Nixon, Brandon, Vivian, Jay L, Soares, Michael J. 2024. Conditionally mutant animal model for investigating the invasive trophoblast cell lineage. In Development (Cambridge, England), 151, . doi:10.1242/dev.202239. https://pubmed.ncbi.nlm.nih.gov/38112206/

4. Kang, Jinwen, Liu, Yingnan, Zhang, Yu, Wu, Yao, Su, Renwei. 2022. The Influence of the Prolactins on the Development of the Uterus in Neonatal Mice. In Frontiers in veterinary science, 9, 818827. doi:10.3389/fvets.2022.818827. https://pubmed.ncbi.nlm.nih.gov/35252420/

5. Green, Madison T, Martin, Rachel E, Kinkade, Jessica A, Mao, Jiude, Rosenfeld, Cheryl S. 2020. Maternal oxycodone treatment causes pathophysiological changes in the mouse placenta. In Placenta, 100, 96-110. doi:10.1016/j.placenta.2020.08.006. https://pubmed.ncbi.nlm.nih.gov/32891007/

6. Outhwaite, J E, Natale, B V, Natale, D R C, Simmons, D G. 2014. Expression of aldehyde dehydrogenase family 1, member A3 in glycogen trophoblast cells of the murine placenta. In Placenta, 36, 304-11. doi:10.1016/j.placenta.2014.12.002. https://pubmed.ncbi.nlm.nih.gov/25577283/