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Table of Contents
Vol. 73, No. 4, 2012
Issue release date: June 2012
Section title: Original Article
Gynecol Obstet Invest 2012;73:277–284
(DOI:10.1159/000333262)

The Expression of Placental Proteoglycans in Pre-Eclampsia

Chui A.a, b · Murthi P.a, b · Brennecke S.P.a, b · Ignjatovic V.c–e · Monagle P.T.c–e · Said J.M.a, b
aDepartment of Perinatal Medicine, Pregnancy Research Centre, The Royal Women’s Hospital, bDepartment of Obstetrics and Gynaecology, The University of Melbourne, and cMurdoch Children’s Research Institute and Departments of dClinical Haematology and ePaediatrics, The Royal Children’s Hospital and The University of Melbourne, Parkville, Vic., Australia

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Article / Publication Details

First-Page Preview
Abstract of Original Article

Received: April 07, 2011
Accepted: September 12, 2011
Published online: April 19, 2012
Issue release date: June 2012

Number of Print Pages: 8
Number of Figures: 4
Number of Tables: 2

ISSN: 0378-7346 (Print)
eISSN: 1423-002X (Online)

For additional information: http://www.karger.com/GOI

Abstract

Background/Aims: Pre-eclampsia (PE) is one of the leading causes of maternal and perinatal morbidity and mortality. PE is defined clinically as the onset of maternal hypertension and proteinuria following 20 weeks of gestation. It is associated with altered maternal uterine decidual spiral artery remodelling, which may lead to reduced blood flow and increased thrombosis within the uteroplacental vasculature. Proteoglycans (PGs) are macromolecules which have (in combination with glycosaminoglycans) important anticoagulant roles in vascular endothelial environments, including the uteroplacental circulation. The hypothesis under consideration in this study was that differential expression of placental PGs may be associated with PE. Methods: PE and control placental samples were collected with ethics approval and patient consent. RNA and protein were extracted and real-time PCR and Western immunoblotting were performed to determine the expression of the PGs in the samples. Results: Of the nine PGs investigated, none showed increased expression, whereas the mRNA and protein expression of five of them was significantly decreased in the placentae of pre-eclamptic women compared to gestation-matched controls. Conclusion: Therefore, the results of this study support the hypothesis that a placental PG deficiency may contribute to the placental thrombotic lesions characteristic of PE.

© 2012 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Article

Received: April 07, 2011
Accepted: September 12, 2011
Published online: April 19, 2012
Issue release date: June 2012

Number of Print Pages: 8
Number of Figures: 4
Number of Tables: 2

ISSN: 0378-7346 (Print)
eISSN: 1423-002X (Online)

For additional information: http://www.karger.com/GOI


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