BMPR2 is required for postimplantation uterine function and pregnancy maintenance. Academic Article uri icon


  • 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.

published proceedings

  • J Clin Invest

altmetric score

  • 10.75

author list (cited authors)

  • Nagashima, T., Li, Q., Clementi, C., Lydon, J. P., DeMayo, F. J., & Matzuk, M. M.

citation count

  • 86

complete list of authors

  • Nagashima, Takashi||Li, Qinglei||Clementi, Caterina||Lydon, John P||DeMayo, Francesco J||Matzuk, Martin M

publication date

  • June 2013