Intracellular calcium ion concentrations in endothelial cells in preeclampsia

  • Matsubara Keiichi
    Department of Obstetrics and Gynecology, Ehime University School of Medicine
  • Mori Miki
    Department of Obstetrics and Gynecology, Ehime University School of Medicine
  • Matsubara Yuko
    Department of Obstetrics and Gynecology, Ehime University School of Medicine
  • Uchikura Yuka
    Department of Obstetrics and Gynecology, Ehime University School of Medicine
  • Nawa Akihiro
    Department of Obstetrics and Gynecology, Ehime University School of Medicine
  • Oka Keizo
    Department of Integrated Center for Science, Ehime University School of Medicine

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Aim: Preeclampsia (PE) is a disorder characterized by hypertensive symptoms and proteinuria in pregnant women. Previous studies have demonstrated that endothelial cell (EC) dysfunction is involved in the pathogenesis of PE. Intracellular free calcium ions are thought to function as secondary messengers in the EC signaling pathway. The aim of this study is to evaluate factors found in sera of PE patients by measuring their effects on intracellular calcium ion concentration ([Ca2+]i) in ECs.<br>Methods: ECs obtained from umbilical cords of normal pregnant women were cultured and incubated with Fura-2/acetoxymethyl ester (Fura-2AM). [Ca2+]i values were measured in ECs treated with sera from 29 normal pregnant women, 7 PE patients, and 10 non-pregnant women by monitoring fluorescence using a CAM 220 fluorometer.<br>Results: [Ca2+]i values were significantly higher in ECs treated with sera from normal pregnant women compared to those from non-pregnant women, and the effects were even stronger when ECs were treated with sera from pregnant women who were in later stages of pregnancy. Furthermore, sera from PE patients significantly increased EC [Ca2+]i compared to those from normal pregnant women in the 3rd trimester.<br>Conclusions: It is possible that serum factors play important roles in the maintenance of normal pregnancy. Furthermore, EC activation could be associated with the pathogenesis of PE through increases in EC [Ca2+]i.

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