Mol. Hum. Reprod. Advance Access published online on March 12, 2009
Molecular Human Reproduction, doi:10.1093/molehr/gap019
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Endometrial cysteine-rich secretory protein 3 is inhibited by human chorionic gonadotropin, and is increased in the decidua of tubal ectopic pregnancy
1Divisions of Reproductive and Developmental Sciences, The University of Edinburgh, Edinburgh, UK 2Pathway Medicine, The University of Edinburgh, Edinburgh, UK 3Pathology, The University of Edinburgh, Edinburgh, UK 4Granulocyte Research Laboratory, Copenhagen University Hospital, Rigshospitalet, Denmark
Corresponding author and reprint requests: Dr Andrew W. Horne, Division of Reproductive and Developmental Sciences, University of Edinburgh, Simpson Centre for Reproductive Health, Royal Infirmary of Edinburgh, 51 Little France Crescent, Edinburgh EH16 4SB, UK, Telephone: +44(0)1312422694, Fax: +44(0)1312422686, E-mail: andrew.horne{at}ed.ac.uk
Ectopic pregnancy (EP) remains a considerable cause of morbidity and occasional mortality. Currently, there is no reliable test to differentiate ectopic from intrauterine gestation. We have previously used array technology to demonstrate that differences in gene expression in decidualised endometrium from women with ectopic and intrauterine gestations could be used to identify candidate diagnostic biomarkers for EP. The aim of this study was to further investigate the decidual gene with the highest fold increase in EP, cysteine-rich secretory protein-3 (CRISP-3). Decidualised endometrium from gestation-matched women undergoing surgical termination of pregnancy (TOP) (n=8), evacuation of uterus for miscarriage (n=6) and surgery for EP (n=11) was subjected to quantitative RT-PCR, morphological assessment, immunohistochemistry and Western blot analysis. Sera were analysed for progesterone and hCG levels. Immortalised endometrial epithelial cells were cultured with physiological concentrations of hCG. CRISP-3 mRNA and protein expression was greater in endometrium from ectopic when compared to intrauterine pregnancies (P<0.05). CRISP-3 protein was localised to epithelium and granulocytes of endometrium. CRISP-3 serum concentrations were not different in women with ectopic compared to intrauterine pregnancies. CRISP-3 expression in endometrium was not related to the degree of decidualisation or to serum progesterone levels. Endometrial CRISP-3 expression was inversely proportional to serum hCG concentrations (P<0.001). Stimulation of endometrial epithelial cells with hCG in vitro caused a reduction in CRISP-3 expression (P<0.01). The measurement of CRISP-3 in endometrium could provide an additional tool in the diagnosis of failing early pregnancy of unknown location. The absence of a local reduction in expression of CRISP-3 in decidualised endometrium of women with EP may be due to reduced exposure to hCG due to the ectopic location of the trophoblast.
Key Words: Ectopic pregnancy/decidualised endometrium/CRISP-3/hCG
Submitted on November 25, 2008; resubmitted on February 25, 2009; accepted on February 27, 2009.
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