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Matrix metalloproteinase-9 deficiency phenocopies features of preeclampsia and intrauterine growth restriction

Plaks, Vicki, (författare)
Department of Anatomy, University of California, San Francisco, CA 94143
Rinkenberger, Julie, (författare)
Department of Anatomy, University of California, San Francisco, CA 94143
Dai, Joanne, (författare)
Department of Anatomy, University of California, San Francisco, CA 94143
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Flannery, Margaret, (författare)
Department of Anatomy, University of California, San Francisco, CA 94143
Sund, Malin, 1972- (författare)
Division of Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115
Kanasaki, Keizo, (författare)
Division of Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115
Ni, Wei, (författare)
Department of Medicine and Diabetes Center, University of California, San Francisco, CA 94143
Kalluri, Raghu, (författare)
Department of Cancer Biology, Metastasis Research Center, University of Texas MD Anderson Cancer Center, Houston, TX 77030
Werb, Zena, (författare)
Department of Anatomy, University of California, San Francisco, CA 94143
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2013
Engelska.
Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 110:27, s. 11109-11114
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • <p>The pregnancy complication preeclampsia (PE), which occurs in approximately 3% to 8% of human pregnancies, is characterized by placental pathologies that can lead to significant fetal and maternal morbidity and mortality. Currently, the only known cure is delivery of the placenta. As the etiology of PE remains unknown, it is vital to find models to study this common syndrome. Here we show that matrix metalloproteinase-9 (MMP9) deficiency causes physiological and placental abnormalities in mice, which mimic features of PE. As with the severe cases of this syndrome, which commence early in gestation, MMP9-null mouse embryos exhibit deficiencies in trophoblast differentiation and invasion shortly after implantation, along with intrauterine growth restriction or embryonic death. Reciprocal embryo transfer experiments demonstrated that embryonic MMP9 is a major contributor to normal implantation, but maternal MMP9 also plays a role in embryonic trophoblast development. Pregnant MMP9-null mice bearing null embryos exhibited clinical features of PE as VEGF dysregulation and proteinuria accompanied by preexisting elevated blood pressure and kidney pathology. Thus, our data show that fetal and maternal MMP9 play a role in the development of PE and establish the MMP9-null mice as a much-needed model to study the clinical course of this syndrome.</p>

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Kirurgi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Surgery (hsv//eng)

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