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Mol. Hum. Reprod. Advance Access originally published online on May 30, 2006
Molecular Human Reproduction 2006 12(7):435-442; 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

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

Julia Francis1, Raj Rai2, Neil J. Sebire3,4, Safaa El-Gaddal2, Maria Sofia Fernandes1, Preeti Jindal2, Amali Lokugamage2, Lesley Regan2 and Jan J. Brosens1,5

1Institute of Reproductive and Developmental Biology, Wolfson & Weston Research Centre for Family Health, Imperial College London, Hammersmith Hospital, 2Department of Obstetrics and Gynaecology, Imperial College London, St Mary’s Hospital, 3Paediatric Malignancy Cytogenetics Unit, Great Ormond Street Hospital for Children, Great Ormond Street and 4Molecular Haematology and Cancer Biology Unit, Institute of Child Health, London, UK

5 To whom correspondence should be addressed at: Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, London W12 0NN, UK. E-mail: j.brosens{at}imperial.ac.uk

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.

Key words: antiphospholipid/complement/decidualization/endometrium/gene expression/miscarriage/pregnancy


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