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Pregnancy-Associated and Placental Proteins in the Placental Tissue Of European Journal of Endocrinology (2002) 147 785–793 ISSN 0804-4643 CLINICAL STUDY Pregnancy-associated and placental proteins in the placental tissue of normal pregnant women and patients with pre-eclampsia at term Nick A Bersinger, Nigel Groome1 and Shanthi Muttukrishna2 Department of Obstetrics and Gynaecology, University of Berne, Berne, Switzerland, 1School of Biological and Molecular Sciences, Oxford Brookes University, Oxford, UK and 2Nuffield Department of Obstetrics and Gynaecology, John Radcliffe Hospital, Oxford, UK (Correspondence should be addressed to N A Bersinger, Reproductive and Perinatal Medicine Research Laboratory, Inselspital G3-855 KKL, Berne, CH-3010, Switzerland; Email: [email protected]) (Shanthi Muttukrishna is currently at Department of Obstetrics and Gynaecology, University College London, Royal Free–UCL Medical School, London WC1E 6HX, UK) Abstract Objective: Pre-eclampsia is a placental disease of unknown cause. Maternal circulating concentrations of a number of protein markers are altered (mainly increased) in pre-eclampsia in comparison with controls of matched gestational age. Inhibin A and activin A were found to be elevated even before the onset of the disease. The aim of this study was to compare the levels of inhibin A, activin A: follistatin ratio, leptin, pregnancy-associated plasma protein-A (PAPP-A), human placental lactogen (HPL), placenta growth factor (PLGF) and pregnancy-specific b1-glycoprotein (SP1) in placental extracts of normal pregnant women and pre-eclampsia patients at term. Methods: Placental tissue from normal pregnancies ðn ¼ 14Þ and patients with pre-eclampsia ðn ¼ 13Þ were collected at term ($37 weeks of gestation) and stored at 280 8C. The frozen tissue pieces were homogenised and the above-mentioned proteins were measured by specific enzyme-linked immunosorbent assays. Results: Placental contents of inhibin A and PAPP-A were significantly higher ðP , 0:05Þ in pre- eclampsia placental extracts compared with the controls. Activin A:follistatin ratio was higher (23) in pre-eclampsia extracts than in the controls (15). Leptin, PLGF, SP1 and HPL levels were not altered in the term pre-eclampsia placenta. Inhibin A and PAPP-A contents were increased in the placental extracts of pre-eclampsia patients. Conclusion: Our data suggest that the placenta, possibly by a compensatory mechanism, is at least in part responsible for the altered serum levels observed in pre-eclampsia. European Journal of Endocrinology 147 785–793 Introduction factor(s), possibly released from the placenta by apoptosis of the syncytiotrophoblast. Pre-eclampsia develops in late pregnancy and may The concentrations of several placental proteins, result in maternal and fetal morbidity and mortality. inflammatory cytokines and growth factors are altered Its cause is as yet unknown. The only treatment for in the maternal circulation of women with pre- pre-eclampsia is the delivery of the placenta, after eclampsia. Inhibins (a–b dimers) and activins (b–b which the symptoms regress rapidly suggesting it is a dimers) are glycoprotein hormones belonging to the placental disease. It is associated with poor placent- transforming-growth factor b superfamily. Follistatin ation with incomplete physiological adaptation of the is a high-affinity activin-binding protein. We and sev- spiral arteries, which prevents them from dilating to eral others have previously shown that the levels of accommodate the increased utero-placental blood activin A (bA–bA dimer) and inhibin A (a–bA flow of late gestation (1). It is believed that the maternal dimer) are significantly elevated in the circulation of syndrome of pre-eclampsia (hypertension, proteinuria, women who have developed pre-eclampsia (3–5), and oedema) results from a generalised inflammatory in women who subsequently develop pre-eclampsia response, which causes maternal endothelial dys- compared with gestational age-matched control preg- function (2). This response is triggered by circulating nant women (6–9). The placenta produces inhibin A q 2002 Society of the European Journal of Endocrinology Online version via http://www.eje.org Downloaded from Bioscientifica.com at 10/01/2021 05:36:36AM via free access 786 N A Bersinger and others EUROPEAN JOURNAL OF ENDOCRINOLOGY (2002) 147 and activin A with a marked increase towards term specifically from the placenta), and the second group (10–12). contains markers that are produced mostly but not The possible occurrence of abnormal serum levels of exclusively by the placenta in pregnancy (PAPP-A, inhi- the ‘new generation’ pregnancy proteins, pregnancy- bin A, activin A, follistatin, PLGF, leptin). Placental associated plasma protein A(PAPP-A) and pregnancy- markers whose levels are reflected in the circulation specific b1-glycoprotein (SP1), have been previously can be useful as biochemical markers of pre-eclampsia studied in detail (for review see 13). Raised PAPP-A before the onset of the disease. concentrations in pre-eclampsia have been reported earlier (14, 15). However, some discrepancy has remained (16) and PAPP-A, as well as SP1, have not Materials and methods been investigated further. Following a preliminary study Placental tissue and extraction (17), we were able to confirm that serum PAPP-A but not SP1 levels were elevated in pre-eclampsia patients Tissue samples were randomly cut from different parts consistent with previous reports (14, 15, 18). of 27 placentae, extensively rinsed in sterile saline, Another hormone with a physiological role outside snap frozen in liquid nitrogen and stored at 280 8C pregnancy but with increased serum levels during ges- at the John Radcliffe Hospital in Oxford, UK. Ethical tation is leptin, the product of the ob gene, which was approval was obtained from the local ethics committee first described in 1994 (19). Leptin is released by peri- for this study. Fourteen of these placentae were from pheral adipocytes (20) and its serum levels correlate control pregnancies at term ($37 weeks of gestation) with body mass (21). In pregnancy, however, it is also and 13 from women with pre-eclampsia at term produced to a considerable extent by the placenta ($37 weeks of gestation). Pre-eclampsia was defined (22), resulting in increasing concentrations with as new, sustained diastolic blood pressure above advancing gestation until the mid-third trimester 90 mmHg and new, sustained proteinuria with (23). It has been suggested that the placenta produces 500 mg protein/24 h urinary sample in the absence of increased amounts of leptin under hypoxic conditions urinary tract infection. Pre-eclamptic patients in this (24). Hence this placental, supposedly body mass- study fitted these criteria. The maternal age was 30:7^ independent fraction of leptin (25) will be of interest 4:9(S.D.) in the control and 30:8^2:7 years in the pre- in the investigation of pre-eclampsia, a condition eclampsia group, and the maternal weight at delivery where there is placental hypoxia. was 88:5^9:5(S.D.) in the control and 88:0^13:5kg Placenta growth factor (PLGF) is a recently described in the pre-eclampsia group. Both groups included five protein, which shares structural and functional proper- primigravidae, and there was no difference in fetal ties with the vascular endothelial growth factor (VEGF). weight, i.e. no infants were diagnosed as small for PLGF, in contrast to VEGF and the above-mentioned gestational age. Labour was uneventful in all cases. markers, was reported to be decreased in the serum of The placental villi (164–559 mg wet weight) were pre-eclampsia patients (26), which could be explained washed twice in 200–400 ml Tris–Cl buffer, 20 mM, by the observation that VEGF was up- and PLGF was pH 7.4, NaCl, 100 mM and homogenised manually in down-regulated by hypoxia in various cancers and four volumes (w/v) of the same buffer containing in vitro in trophoblast-derived cell lines (27, 28). The EDTA-free serine-/cysteine-protease inhibitor cocktail similarities between PLGF and VEGF, which are (Roche Biochemicals, diluted according to the manu- mainly produced by endothelial cells besides its syn- facturer’s instructions) in a serrated glass–Teflon thesis in the trophoblast (29), render an assignment homogeniser. The supernatant extract was collected of PLGF production exclusively to the placenta in after centrifugation (6000 g,20min,48C) and the pregnant women rather improbable. total protein concentration determined with the Brad- Maternal endothelial cell dysfunction is thought to ford assay (Pierce, Lausanne, Switzerland) using be responsible for the observed life-threatening symp- human serum albumin as a standard. Extracts were toms of pre-eclampsia (30, 31). Nevertheless, it is divided into two to three aliquots and stored at speculated that the placenta is at the origin of the 240 8C until quantitative analyses were performed in disease with insufficient trophoblast invasion and its batch. consequences on vasculogenesis and oxygen delivery. Most studies have reported changes in placenta-derived Analytical assay methods factors in the maternal circulation. We have set out to investigate if there is any difference in the placental All proteins were quantified in the extracts using content of trophoblast-specific and associated markers double-antibody enzyme-linked immunosorbent assays in pre-eclampsia compared with normal pregnancies. (ELISA) based on 96-well plates. The methods were fol- Activin A was recently reported to be increased in lowing either two-incubation (enzyme-labelled second placental (but not in other gestational) tissue of pre- antibody) or three-incubation (biotinylated second eclampsia patients (32). Our first group included SP1 antibody followed by streptavidin–enzyme conjugate) and human placental lactogen (HPL, originating protocols, with washing steps using phosphate-buffered www.eje.org Downloaded from Bioscientifica.com at 10/01/2021 05:36:36AM via free access EUROPEAN JOURNAL OF ENDOCRINOLOGY (2002) 147 Placental tissue proteins in pre-eclampsia 787 saline (PBS) containing Tween-20 (Sigma) at 0.1% Activin A (v/v) (PBST) between steps. Activin A was measured using a two-site ELISA as described before (12).
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