Journal
PLACENTA
Volume 35, Issue 2, Pages 117-124Publisher
W B SAUNDERS CO LTD
DOI: 10.1016/j.placenta.2013.11.008
Keywords
Clinical severity; Decidua; Gene expression; Pre-eclampsia; Susceptibility genes
Funding
- Royal Women's Hospital, Parkville, Australia
- National Institutes of Health [HD049847]
- University of Melbourne's Melbourne International Fee Remission Scholarship
- Felix Meyer Scholarship in Obstetrics and Gynaecology
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Introduction: Pre-eclampsia (PE) has a familial association, with daughters of women who had PE during pregnancy having more than twice the risk of developing PE themselves. Through genome-wide linkage and genetic association studies in PE-affected families and large population samples, we previously identified the following as positional candidate maternal susceptibility genes for PE; ACVR1, INHA, INHBB, ERAP1, ERAP2, LNPEP, COL4A1 and COL4A2. The aims of this study were to determine mRNA expression levels of previously identified candidate maternal pre-eclampsia susceptibility genes from normotensive and severe PE (SPE) pregnancies and correlate mRNA expression levels with the clinical severity of SPE. Methods: Third trimester decidual tissues were collected from both normotensive (n = 21) and SPE pregnancies (n = 24) and mRNA expression levels were determined by real-time PCR. Gene expression was then correlated with several parameters of clinical severity in SPE. Statistical significance was determined by Mann Whitney U test and Spearman's Correlation. Results: The data demonstrate significantly increased decidual mRNA expression levels of ACVR1, INHBB, ERAP1, ER4P2, LNPEP, COL4A1 and COL4A2 in SPE (p < 0.05). Increased mRNA expression levels of several genes INHA, INHBB, COL4A1 and COL4A2 were correlated with earlier onset of PE and earlier delivery of the fetus (p < 0.05). Conclusion: These results suggest altered expression of maternal susceptibility genes may play roles in PE development and the course of disease severity. (C) 2013 Elsevier Ltd. All rights reserved.
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