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Overexpression of CD39 protects in a mouse model of preeclampsia

Authors

  • Jennifer L McRae,

    Corresponding author
    • Immunology Research Centre, St. Vincent's Hospital, Melbourne, Victoria, Australia
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  • Prudence A Russell,

    1. Department of Anatomical Pathology, St. Vincent's Hospital, Melbourne, Victoria, Australia
    2. Department of Pathology, University of Melbourne, Melbourne, Victoria, Australia
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  • Joanne SJ Chia,

    1. Immunology Research Centre, St. Vincent's Hospital, Melbourne, Victoria, Australia
    2. Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia
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  • Karen M Dwyer

    1. Immunology Research Centre, St. Vincent's Hospital, Melbourne, Victoria, Australia
    2. Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia
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Correspondence:

Dr Jennifer McRae, Immunology Research Centre, St. Vincent's Hospital, Melbourne, Fitzroy 3065, Vic., Australia. Email: jennifer.mcrae@svhm.org.au

Abstract

CD39 (NTPDase1), a critical immune and vascular ecto-nucleotidase, hydrolyses pro-inflammatory and pro-thrombotic nucleotides (adenosine-5′-triphosphate (ATP) and adenosine diphosphate) to adenosine. In humans, CD39 is the dominant ecto-nucleotidase in placental trophoblastic tissues and modulates ATP-dependent trophoblastic functions. CD39 is an integral component of regulatory T cells (Treg), which are central to immunological tolerance and maintenance of normal pregnancy. We examined the impact of CD39 overexpression in a mouse model of preeclampsia. Matings were performed between virginal BALB/c female (wild-type (WT) or CD39 transgenic (CD39TG)) and C57BL/6 male mice. On days 10 and 12 of pregnancy BALB/c Th1-polarized cells were injected. Systolic blood pressure (SBP) was measured throughout pregnancy. Mice were sacrificed at day 15 of pregnancy. Following transfer of Th1-polarized cells, SBP of pregnant WT mice increased (118 ± 3 mmHg to 142 ± 5 mmHg). Although ultrastructural changes were evident in the kidney this was not accompanied by significant proteinuria. SBP remained unchanged (115 ± 2 mmHg to 114 ± 3 mmHg) in pregnant CD39TG mice without evidence of renal lesions. We conclude that gestational hypertension can be induced in mice following transfer of maternally derived Th1-polarized cells and that overexpression of CD39 is protective in this model.

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