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  • Title: PP168. The role of calcium supplementation in prevention endothelial cell activation, and possible relevance to preeclampsia.
    Author: Chen Q, Tong M, Wu M, Stone P, Snowise S, Chamley L.
    Journal: Pregnancy Hypertens; 2012 Jul; 2(3):330. PubMed ID: 26105489.
    Abstract:
    INTRODUCTION: Preeclampsia remains a leading causing of maternal and perinatal mortality and morbidity. Preeclampsia is currently thought to be primarily a disease of endothelial activation and inflammation. OBJECTIVES: The deportation of trophoblast debris form the placenta was first linked to the pathogenesis of preeclampsia over a hundred years ago and it is hypothesised that deportation of necrotic trophoblast debris may contribute to maternal endothelial cell activation in preeclampsia. We have previously shown that treating placental explants with IL-6 results in shedding of more necrotic trophoblast debris from placental explants and that this debris when phagocytosed by endothelial cells results in activation of the endothelial cells. Although delivery remains the only definitive cure for preeclampsia a number of studies suggest that calcium supplementation may reduce the risk of developing preeclampsia by up to 50% but the protective mechanism of calcium supplementation is unclear. The aim of this work was to determine whether calcium supplementation affects either the production of necrotic trophoblast debris from the placenta or influences endothelial cell activation. METHODS: First trimester placental explants were cultured with IL-6 in the presence or absence of increasing concentrations of calcium (CaCl2) for 24h. Trophoblastic debris was collected from the explants and then exposed to monolayers of endothelial cell for 24h and endothelial cell activation measured by ICAM-1 ELISA. In other experiments, endothelial cells were treated with IL-6 or necrotic trophoblastic debris in the presence of increasing concentrations of CaCl2, ranging from 230μg/mL to 700μg/mL, for 24h. In some experiments, ebdothelial cells were treated with low concentration of CaCl2, ranging from 0μg/mL to 230μg/mL for 24h. Endothelial cell activation was measured by quantifying cell-surface ICAM-1 levels by ELISA. CONCLUSION: Our results demonstrate that calcium levels are important to endothelial cell activation and supplemental calcium may reverse the activation of the endothelium induced by proinflammatory mediators while having no effect on the production of trophoblast debris. These results may in part help to explain the benefits of calcium supplementation in the reduction of risk for developing preeclampsia.
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