Abstract
The endometrial gland is one of the most important components of the mammalian uterus. However, few studies have been conducted on the regulatory mechanisms of adenogenesis during the development of endometrium. In the present study, we detected the genes expression of 35 different prolactin family members (PRLs) together with the prolactin receptor (PRL-R) in the endometrium of neonatal mice along with the adenogenesis process, to address which prolactin-like genes play a key role during gland development in mice. We found that: (1) The expression of Prl1a1, Prl3d1, Prl5a1, Prl7a1, Prl7a2, Prl7d1, Prl8a6, Prl8a8, and Prl8a9 genes were significantly increased along with the development of uterine glands. Prl7c1 and Prl8a1 were observably up-regulated on Postnatal day 5 (PND5) when the uterine glandular bud invagination begins. Prl3a1, Prl3b1, and Prl7b1 suddenly increased significantly on PND9. But, Prl3c1 and Prl8a2 were markedly down-regulated on PND5 and the expression of Prl6a1 and Prlr were stable extremely. (2) After continuous injection of Progesterone (P4), a well-known method to suppress the endometrial adenogenesis, the expression of Prl1a1, Prl3d1, Prl5a1, Prl7a1, Prl7a2, Prl7d1, Prl8a6, Prl8a8, Prl8a9, and Prlr were suppressed on PND7. And on PND9, Prl1a1, Prl3d1, Prl8a6, Prl8a8, and Prl8a9 were significantly inhibited. (3) Further analysis of the epithelial and stroma showed that these PRLs were mainly expressed in the endometrial stroma of neonatal mice. Our results indicate that multiple PRLs are involved in uterine development and endometrial adenogenesis. Continued progesterone therapy may alter the expression pattern of these PRLs in endometrial stromal cells, thereby altering the interaction and communication between stroma and epithelium, and ultimately leading to complete suppression of endometrial adenogenesis.
Highlights
The uterus is a key reproductive organ for female mammals to reproduce offspring
Prl7c1 and Prl8a1 were observably up-regulated at uterine glandular buds invagination (PND5), and slightly down-regulated on PND7 and PND9, but their expression levels were still stronger than those on PND3 (Figure 3A)
Prl3c1 and Prl8a2 were markedly down-regulated on Postnatal day 5 (PND5), and Prl3c1 subsequently recovered to the expression level of PND3 on PND7 and PND9, while Prl8a2 was still down-regulated on PND7, and recovered to the expression level of PND3 on PND9 (Figure 3C)
Summary
The uterus is a key reproductive organ for female mammals to reproduce offspring. In mammals, the uterus develops from the accessory middle renal tube, or Mueller’s tube, which gives rise to the funnel, fallopian tube, uterus, cervix, and vaginal vestibule [1]. Leukemia inhibitory factor (LIF) and calcitonin are two important secretions of the uterine glands that are essential for the establishment of uterine receptivity and embryo implantation [5]. LIF expression is induced by estrogen on day 4 of gestation and is secreted into the endometrial cavity, regulating embryo implantation and decidualization. The knockout of LIF in the mouse uterus leads to the failure of embryo implantation, and further results in pregnancy failure [6]. Calcitonin, a peptide hormone that regulates calcium homeostasis, is secreted by the endometrial glandular epithelium on day 2 of gestation in mice and peaks the day before implantation (Day 4) to regulate embryo implantation [7]. Calcitonin modulates the expression of certain genes in the endometrium, including down-regulating the E-cadherin expression in rodent uterine epithelium [8]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
