PP168. The role of calcium supplementation in prevention endothelial cell activation, and possible relevance to preeclampsia.

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dc.contributor.author Chen, Qi en
dc.contributor.author Tong, M en
dc.contributor.author Wu, M en
dc.contributor.author Stone, Peter en
dc.contributor.author Snowise, S en
dc.contributor.author Chamley, Lawrence en
dc.date.accessioned 2018-10-10T04:10:33Z en
dc.date.issued 2012-07 en
dc.identifier.issn 2210-7789 en
dc.identifier.uri http://hdl.handle.net/2292/40475 en
dc.description.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. RESULTS: 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. en
dc.format.medium Print-Electronic en
dc.relation.ispartofseries Pregnancy hypertension en
dc.rights Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. en
dc.rights.uri https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm en
dc.title PP168. The role of calcium supplementation in prevention endothelial cell activation, and possible relevance to preeclampsia. en
dc.type Conference Item en
dc.identifier.doi 10.1016/j.preghy.2012.04.279 en
pubs.issue 3 en
pubs.begin-page 330 en
pubs.volume 2 en
dc.rights.holder Copyright: The author en
dc.identifier.pmid 26105489 en
pubs.publication-status Published en
dc.rights.accessrights http://purl.org/eprint/accessRights/RestrictedAccess en
pubs.elements-id 489034 en
pubs.org-id Medical and Health Sciences en
pubs.org-id School of Medicine en
pubs.org-id Obstetrics and Gynaecology en
dc.identifier.eissn 2210-7797 en
pubs.record-created-at-source-date 2015-06-24 en
pubs.dimensions-id 26105489 en


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