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Mol. Hum. Reprod. Advance Access published online on May 30, 2006
Molecular Human Reproduction, doi:10.1093/molehr/gal048
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© The Author 2006. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received March 1, 2006
Accepted April 23, 2006

Article

Impaired expression of endometrial differentiation markers and complement regulatory proteins in patients with recurrent pregnancy loss associated with antiphospholipid syndrome

Julia Francis 1, Raj Rai 2, Neil J. Sebire 3, Safaa El-Gaddal 2, Maria Sofia Fernandes 1, Preeti Jindal 2, Amali Lokugamage 2, Lesley Regan 2, and Jan J. Brosens 1 *

1 Institute of Reproductive and Developmental Biology, Wolfson & Weston Research Centre for Family Health, Imperial College London, Hammersmith Hospital, London, UK
2 Department of Obstetrics and Gynaecology, Imperial College London, St Mary’s Hospital, London, UK
3 Paediatric Malignancy Cytogenetics Unit, Great Ormond Street Hospital for Children, Great Ormond Street; Molecular Haematology and Cancer Biology Unit, Institute of Child Health, London, UK

* To whom correspondence should be addressed.
Jan J. Brosens, E-mail: j.brosens{at}imperial.ac.uk


  Abstract

Antiphospholipid syndrome (APS), characterized by circulating antiphospholipid (aPL) antibodies, is a major cause of early pregnancy failure and placental insufficiency. In this study, we examined whether impaired endometrial differentiation before conception contributes to the high incidence of pregnancy complications in APS. Timed secretory endometrial biopsies were obtained from a cohort of women with recurrent pregnancy loss (RPL). Real-time quantitative (RTQ)-PCR was used to determine the expression levels of transcripts that encode for decidual markers, proinflammatory cytokines and complement regulatory proteins. Expression of decidual markers such as prolactin (PRL), tissue factor (TF) and signal transducer and activator of transcription 5 (Stat5), but not insulin-like growth factor-binding protein 1 (IGFBP-1), was significantly lower in samples obtained from aPL+ patients (n = 24) when compared with aPL- group (n = 58) (P < 0.05). The abundance of transcripts encoding for interferon {gamma} (IFN{gamma}), tumour necrosis factor {alpha} (TNF{alpha}) or Stat1 did not differ significantly between both groups (P ≥ 0.05). However, analysis of transcripts that encode for complement regulatory proteins showed a marked decrease in decay-accelerating factor (DAF/CD55) levels in aPL+ patients (P = 0.005), which was mimicked at protein level as demonstrated by immunohistochemistry. In summary, patients with RPL have distinct endometrial gene expression profiles depending on the presence or absence of circulating aPL antibodies. In APS, impaired endometrial differentiation and lower DAF/CD55 expression before conception may compromise implantation and predispose to complement-mediated pregnancy failure.

Keywords: antiphospholipid/complement/decidualization/endometrium/gene expression/miscarriage/pregnancy.
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