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Overexpression of CD39 protects in a mouse model of preeclampsia
journal contribution
posted on 2013-05-01, 00:00 authored by Jennifer L McRae, Prudence A Russell, Joanne Sj Chia, Karen DwyerKaren DwyerCD39 (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.
History
Journal
NephrologyVolume
18Issue
5Pagination
351 - 355Publisher
WileyLocation
London, Eng.Publisher DOI
eISSN
1440-1797Language
engPublication classification
C1 Refereed article in a scholarly journalCopyright notice
2013, The AuthorsUsage metrics
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AnimalsAntigens, CDApyraseCell PolarityFemaleMaleMiceMice, Inbred BALB CMice, Inbred C57BLPre-EclampsiaPregnancySystoleTh1 CellsScience & TechnologyLife Sciences & BiomedicineUrology & NephrologyadenosinehypertensionNTPDase1preeclampsiaISCHEMIA-REPERFUSION INJURYT-CELLSPREGNANT RATSEXPRESSIONSUPPRESSIONECLAMPSIARECEPTOR
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