Document Detail


BMPR2 is required for postimplantation uterine function and pregnancy maintenance.
MedLine Citation:
PMID:  23676498     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Takashi Nagashima; Qinglei Li; Caterina Clementi; John P Lydon; Francesco J DeMayo; Martin M Matzuk
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2013-05-08
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  123     ISSN:  1558-8238     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  2013 Jun 
Date Detail:
Created Date:  2013-05-31     Completed Date:  2013-08-02     Revised Date:  2014-05-12    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2539-50     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Angiopoietins / metabolism
Animals
Bone Morphogenetic Protein Receptors, Type II / genetics*,  metabolism,  physiology
Cell Differentiation
Cell Proliferation
Decidua / immunology,  metabolism*,  pathology
Embryo Implantation*
Estradiol / blood
Female
Fetal Growth Retardation / genetics
Gene Expression
Giant Cells / pathology
Infertility, Female / genetics
Interleukin-15 / metabolism
Killer Cells, Natural / physiology
Male
Mice
Mice, 129 Strain
Mice, Inbred C57BL
Mice, Knockout
Placenta / blood supply,  pathology
Pregnancy
Pregnancy Maintenance*
Progesterone / blood
Serine Endopeptidases / metabolism
Signal Transduction
Trophoblasts / pathology
Uterus / immunology,  metabolism,  physiopathology
Vascular Endothelial Growth Factor A / metabolism
Grant Support
ID/Acronym/Agency:
CA077530/CA/NCI NIH HHS; HD032067/HD/NICHD NIH HHS; R01 HD032067/HD/NICHD NIH HHS; R01HD042311/HD/NICHD NIH HHS; U54HD007495/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Angiopoietins; 0/Interleukin-15; 0/Vascular Endothelial Growth Factor A; 0/vascular endothelial growth factor A, mouse; 4G7DS2Q64Y/Progesterone; 4TI98Z838E/Estradiol; EC 2.7.11.30/Bmpr2 protein, mouse; EC 2.7.11.30/Bone Morphogenetic Protein Receptors, Type II; EC 3.4.21.-/Corin protein, mouse; EC 3.4.21.-/Serine Endopeptidases
Comments/Corrections
Comment In:
Nat Rev Endocrinol. 2013 Jul;9(7):380   [PMID:  23689817 ]

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