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Differential gene expression at the maternal-fetal interface in preeclampsia is influenced by gestational age.

ABSTRACT: Genome-wide transcription data of utero-placental tissue has been used to identify altered gene expression associated with preeclampsia (PE). As many women with PE deliver preterm, there is often a difference in gestational age between PE women and healthy pregnant controls. This may pose a potential bias since gestational age has been shown to dramatically influence gene expression in utero-placental tissue. By pooling data from three genome-wide transcription studies of the maternal-fetal interface, we have evaluated the relative effect of gestational age and PE on gene expression. A total of 18,180 transcripts were evaluated in 49 PE cases and 105 controls, with gestational age ranging from week 14 to 42. A total of 22 transcripts were associated with PE, whereas 92 transcripts with gestational age (nominal P value <1.51*10(-6), Bonferroni adjusted P value <0.05). Our results indicate that gestational age has a great influence on gene expression both in normal and PE-complicated pregnancies. This effect might introduce serious bias in data analyses and needs to be carefully assessed in future genome-wide transcription studies.

SUBMITTER: Lian IA

PROVIDER: S-EPMC3729459 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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Differential gene expression at the maternal-fetal interface in preeclampsia is influenced by gestational age.

Lian Ingrid A IA Langaas Mette M Moses Eric E Johansson Åsa Å

PloS one 20130731 7

Genome-wide transcription data of utero-placental tissue has been used to identify altered gene expression associated with preeclampsia (PE). As many women with PE deliver preterm, there is often a difference in gestational age between PE women and healthy pregnant controls. This may pose a potential bias since gestational age has been shown to dramatically influence gene expression in utero-placental tissue. By pooling data from three genome-wide transcription studies of the maternal-fetal inte ...[more]

PMID: 23936112

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Project description:ImportanceIt remains unknown whether neurodevelopmental impairments are directly associated with the structural development of the brain in offspring with fetal growth restriction (FGR) and mothers with preeclampsia (PE) or gestational hypertension (GH).ObjectivesTo assess whether fetal corpus callosum (CC) development differed among pregnancies with PE or GH with FGR, pregnancies with PE or GH without FGR, and normotensive pregnancies, particularly the severity of maternal disease and FGR, and to identify the association between adverse perinatal outcomes and structural development of the CC in fetuses with FGR in pregnancies with PE or GH.Design, setting, and participantsThis retrospective matched case-control study was conducted between January 1, 2014, and January 31, 2021, at Women's Hospital, Zhejiang University School of Medicine in Hangzhou, China. The participant group included cases of singleton pregnancies with PE or GH with FGR; the control groups included cases with PG or GH without FGR and cases with paired normotensive pregnancy.ExposuresMaternal PE or GH and FGR.Main outcomes and measuresThe length, thickness, total area, subdivision areas, and apparent diffusion coefficient (ADC) values of fetal CC were measured on magnetic resonance imaging (MRI) and analyzed. The association between adverse perinatal outcomes and structural development of CC was further investigated.ResultsA total of 56 pregnant individuals with singleton pregnancies and PE or GH and fetuses with FGR were enrolled (maternal median [IQR] age, 29.0 [26.0-34.0] years; mean [SD] gestational age at MRI, 33.6 [2.5] weeks). Significant patterns of decreased median (IQR) fetal CC length (0.4284 [0.4079-0.4470] mm vs 0.4614 [0.4461-0.4944] mm, P < .001, vs 0.4591 [0.4310-0.4927] mm, P < .001) and mean (SD) CC total area (1.0779 [0.1931] mm2 vs 1.1896 [0.1803] mm2, P = .001, vs 1.1438 [0.1935] mm2, P = .02), adjusted for the cephalic index, was observed in cases of PE or GH with FGR compared with cases without FGR and cases with normotensive pregnancy. The splenium region of fetal CC also exhibited the distinct alterations in macrostructural development (with FGR: 0.3149 [0.0697] mm2 vs without FGR: 0.3727 [0.0698] mm2, P < .001, vs normotensive pregnancies: 0.3565 [0.0763] mm2, P < .001) and microstructural development (median [IQR] ADC values: 1.47 [1.38-1.57] × 10-3 mm2/s vs 1.57 [1.53-1.63] × 10-3 mm2/s, P = .009, vs 1.63 [1.50-1.70] × 10-3 mm2/s, P < .001) in all groups. Furthermore, significant associations were found between structural abnormality of the splenium region and adverse perinatal outcomes in the PE or GH with FGR group (mean [SD] ADC value: 1.40 [0.07] × 10-3 mm2/s; P = .04).Conclusions and relevanceResults of this study suggest that, in fetuses with FGR in pregnancies with PE or GH, decreased structural development of the CC, predominantly the splenium region, may be significantly associated with a higher risk of adverse perinatal outcomes and may be regarded as an MRI-based biomarker for better prenatal counseling and early management decisions.

Project description:Preeclampsia (PE), which affects 4-8% of human pregnancies, causes significant maternal and neonatal morbidity and mortality. Within the basal plate, placental cytotrophoblasts (CTBs) of fetal origin invade the uterus and extensively remodel the maternal vasculature. In PE, CTB invasion is often shallow, and vascular remodeling is rudimentary. To better understand possible causes, we conducted a global analysis of gene expression at the maternal-fetal interface in placental samples from women with PE (n = 12; 24-36 wk) vs. samples from women who delivered due to preterm labor with no evidence of infection (n = 11; 24-36 wk), a condition that our previous work showed is associated with normal CTB invasion. Using the HG-U133A&B Affymetrix GeneChip platform, and statistical significance set at log odds-ratio of B >0, 55 genes were differentially expressed in PE. They encoded proteins previously associated with PE [e.g. Flt-1 (vascular endothelial growth factor receptor-1), leptin, CRH, and inhibin] and novel molecules [e.g. sialic acid binding Ig-like lectin 6 (Siglec-6), a potential leptin receptor, and pappalysin-2 (PAPP-A2), a protease that cleaves IGF-binding proteins]. We used quantitative PCR to validate the expression patterns of a subset of the genes. At the protein level, we confirmed PE-related changes in the expression of Siglec-6 and PAPP-A2, which localized to invasive CTBs and syncytiotrophoblasts. Notably, Siglec-6 placental expression is uniquely human, as is spontaneous PE. The functional significance of these novel observations may provide new insights into the pathogenesis of PE, and assaying the circulating levels of these proteins could have clinical utility for predicting and/or diagnosing PE. Keywords: disease state analysis Basal plate biopsies of preterm labor (24-36 weeks; n=11) and preterm severe preeclampsia (24-36 weeeks; n=12) were isolated and the global gene expression profiles determined using Affymetrix Human GeneChips. Comparisons between the preeclampsia samples and the preterm labor controls revealed genes differentially expressed in preeclampsia.

Dataset Information

Differential gene expression at the maternal-fetal interface in preeclampsia is influenced by gestational age.

Publications

Differential gene expression at the maternal-fetal interface in preeclampsia is influenced by gestational age.

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