| First Author | Nagashima T | Year | 2013 |
| Journal | J Clin Invest | Volume | 123 |
| Issue | 6 | Pages | 2539-50 |
| PubMed ID | 23676498 | Mgi Jnum | J:201437 |
| Mgi Id | MGI:5514105 | Doi | 10.1172/JCI65710 |
| Citation | Nagashima T, et al. (2013) BMPR2 is required for postimplantation uterine function and pregnancy maintenance. J Clin Invest 123(6):2539-50 |
| abstractText | Abnormalities in cell-cell communication and growth factor signaling pathways can lead to defects in maternal-fetal interactions during pregnancy, including immunologic rejection of the fetal/placental unit. In this study, we discovered that bone morphogenetic protein receptor type 2 (BMPR2) is essential for postimplantation physiology and fertility. Despite normal implantation and early placental/fetal development, deletion of Bmpr2 in the uterine deciduae of mice triggered midgestation abnormalities in decidualization that resulted in abnormal vascular development, trophoblast defects, and a deficiency of uterine natural killer cells. Absence of BMPR2 signaling in the uterine decidua consequently suppressed IL-15, VEGF, angiopoietin, and corin signaling. Disruption of these pathways collectively lead to placental abruption, fetal demise, and female sterility, thereby placing BMPR2 at a central point in the regulation of several physiologic signaling pathways and events at the maternal-fetal interface. Since trophoblast invasion and uterine vascular modification are implicated in normal placentation and fetal growth in humans, our findings suggest that abnormalities in uterine BMPR2-mediated signaling pathways can have catastrophic consequences in women for the maintenance of pregnancy. |
