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BMPR2 is required for postimplantation uterine function and pregnancy maintenance.
|Title||BMPR2 is required for postimplantation uterine function and pregnancy maintenance.|
|Publication Type||Journal Article|
|Year of Publication||2013|
|Authors||Nagashima T, Li Q, Clementi C, Lydon JP, Demayo FJ, Matzuk MM|
|Journal||The Journal of clinical investigation|
|Date Published||2013 Jun 3|
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.
|Alternate Journal||J. Clin. Invest.|