Different expression profiles of mRNAs in preeclampsia and normal placenta (mRNA)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE149812 | GEO | 2023/04/23
REPOSITORIES: GEO
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Project description:Preeclampsia (PE), which results from abnormal placentation, acts as a primary cause of maternal and neonatal morbidity and mortality. However, the cause of abnormal development of placenta remain poorly understood. BHLHE40, a transcript factor, is up-regulated in PE placenta compared to normal placenta probably due to the stimulation by low oxygen, but the implication of BHLHE40 in PE pathogenesis is not elucidated. Therefore, we conducted transcriptional profiling of genes in HTR-8/Svneo cells with BHLHE40 knockdown or not.
2023-04-23 | GSE150113 | GEO
Project description:Preeclampsia complicates more than 3% of all pregnancies in the United States and Europe. High-risk populations include women with diabetes, dyslipidemia, thrombotic disorders, hyperhomocysteinemia, hypertension, renal diseases, previous preeclampsia, twin pregnancies, and low socioeconomic status. In the latter case, the incidence may increase to 20% to 25%. Preeclampsia is a major cause of maternal and fetal morbidity and mortality. Preeclampsia is defined by systolic blood pressure of more than 140 mm Hg and diastolic blood pressure of more than 90 mm Hg after 20 weeks gestation in a previously normotensive patient, and new-onset proteinuria. Abnormal placentation associated with shallow trophoblast invasion (fetal cells from outer cell layer of the blastocyst) into endometrium (decidua) and improper spiral artery remodeling in the decidua are initial pathological steps. In this study we analyzed the renin-angiotensin system in adipose tissue, decidua and placenta from women with uneventful pregnancy and women with preeclampsia. We also analyzed the tissue by Affymetrix chips in a comparison study (control vs. preeclampsia) Experiment Overall Design: 6 affymetrix human expression chips (GPL570) were analyzed. Experiment Overall Design: They represent 3 tissues (pooled from 10 individuals each) from patients with preeclampsia and from patients with uneventful pregnancy (collected by cesaraen section). Tissues from patients with uneventful pregnancy are the controls in comparison to tissues of patients with preeclampsia.
2008-06-14 | E-GEOD-6573 | biostudies-arrayexpress
Project description:Defective deep placentation, an abnormal transformation of the spiral arteries in the junctional zone of the myometrium, is known to cause significant obstetrical complications such as preeclampsia (PE), fetal growth restriction, and placental infarcts with fetal death. Serological biomarkers to predict and diagnose PE would help antenatal care and reduce the obstetrical complications. To discover biomarkers for prediction of PE, we first performed global proteome profiling of three pairs of maternal plasma samples obtained from the early second trimester pregnant women who subsequently developed PE and controls to identify proteins that were abundant in the patients. We further evaluated the expression changes of PE representing proteins in stored plasma samples of a cohort of subsequently developed PE and their matched controls by MRM assay. We identified both Complement C1s subcomponent (p-value = 0.041) and Protein AMBP (p-value = 0.043) were up-regulated in the cohort of PE plasma samples before manifestation of clinical disease. We propose that these proteins may be involved in the remodeling process of the spiral arteries even before the manifestation of PE. These proteins could be served as potential plasma biomarkers to predict pregnant women at increased risk of developing PE.
2018-07-05 | PXD003419 | Pride
Project description:Background: Long non-coding RNAs (lncRNAs) are an important class of pervasive genes involved in a variety of biological functions. They are aberrantly expressed in many types of diseases. We want to study the lncRNAs profiles in preeclampsia. Preeclampsia has been observed in patients with molar pregnancy where a fetus is absent demonstrating that the placenta is sufficient to cause the condition. So we analyze the lncRNAs profiles in preeclampsia placentas. In this study, we described the lncRNAs profiles in 6 preeclampsia placentas (T) and 5 matched normal pregnancy placentas (N) tissues by microarray. Methodology/Principal Findings: With abundant and varied probes accounting 33,045 LncRNAs in our microarray, the number of lncRNAs that expressed at a certain level could be detected is 28,443. From the data we found there were 738 lncRNAs that differentially expressed (M-bM-^IM-%1.5 fold-change) among preeclampsia placentas compared with matched controls. Up to 18,063 coding transcripts could be detected in placenta samples through 30,215 coding transcripts probes. Coding-non-coding gene co-expression networks (CNC network) were constructed based on the correlation analysis between the differential expressed lncRNAs and mRNAs. According to the GO-Pathway analysis of differential expressed lncRNAs/mRNAs, we choose three lncRNAs to analyze the relationship between lncRNAs and preeclampsia. LOC391533, LOC284100, CEACAMP8 were evaluated by qPCR in 40 of preeclampsia placentas and 40 of controls. The results showed three lncRNAs were aberrantly expressed in preeclampsia placentas compared with controls. Conclusions/Significance: Our study is the first one to determine genome-wide lncRNAs expression patterns in preeclampsia placenta by microarray. The results displayed that clusters of lncRNAs were aberrantly expressed in preeclampsia placenta compared with controls, which revealed that lncRNAs differentially expressed in preeclampsia placenta may exert a partial or key role in preeclampsia development. Misregulation of LOC391533, LOC284100, CEACAMP8 might be associated with preeclampsia. Taken together, this study may provide potential targets for future treatment of preeclampsia and novel insights into preeclampsia biology. LncRNAs/mRNAs profiles in 6 preeclampsia placentas and 5 matched normal pregnancy placentas tissues by microarray using Arraystar v2.0.
2013-09-12 | E-GEOD-50783 | biostudies-arrayexpress
Project description:Preeclampsia (PE) is the leading cause of prenatal morbidity and mortality. It is associated with defective trophoblast functions at implantation, but manifestation of its phenotypes is in late pregnancy. There is no reliable method for early prediction and treatment of PE. Adrenomedullin (ADM) is an abundant placental peptide in early pregnancy. Here, integrated single-cell sequencing and spatial transcriptomics confirm a high ADM expression in the human villous cytotrophoblast. The levels of ADM in chorionic villi and serum were lower in first-trimester pregnant women who later developed PE than those with normotensive pregnancy. ADM stimulates differentiation of trophoblast stem cells and trophoblast organoids in vitro. In pregnant mice, placenta-specific ADM suppression led to PE-like phenotypes. The PE-like phenotypes in a mouse PE model were reduced by a novel placenta-specific nanoparticle-based forced expression of ADM. Our study reveals the roles of trophoblastic ADM in placental development, PE pathogenesis and its potential clinical uses.
2023-07-09 | GSE236475 | GEO
Project description:Preeclampsia (PE) is a hypertensive pregnancy disorder with increased risk of maternal and fetal morbidity and mortality. Abnormal extravillous trophoblast (EVT) development and function is considered to be the underlying cause of PE, but has not previously been modeled in vitro. We previously derived induced pluripotent stem cells (iPSC) from placentas of PE patients and characterized abnormalities in formation of syncytiotrophoblast and responses to changes in oxygen tension. In this study, we converted these primed iPSC to naïve iPSC, then derived trophoblast stem cells (TSC) and EVT to evaluate molecular mechanisms underlying PE. We found that primed (but not naïve) iPSC-derived PE-EVT have reduced surface HLA-G, blunted invasive capacity, and altered EVT-specific gene expression. These abnormalities correlated with promotor hypermethylation of genes associated with the epithelial-mesenchymal transition pathway, specifically in primed-iPSC derived PE-EVT. Our findings indicate that abnormal epigenetic regulation might play a role in the PE pathogenesis.
2024-03-27 | GSE243579 | GEO
Project description:Preeclampsia complicates more than 3% of all pregnancies in the United States and Europe. High-risk populations include women with diabetes, dyslipidemia, thrombotic disorders, hyperhomocysteinemia, hypertension, renal diseases, previous preeclampsia, twin pregnancies, and low socioeconomic status. In the latter case, the incidence may increase to 20% to 25%. Preeclampsia is a major cause of maternal and fetal morbidity and mortality. Preeclampsia is defined by systolic blood pressure of more than 140 mm Hg and diastolic blood pressure of more than 90 mm Hg after 20 weeks gestation in a previously normotensive patient, and new-onset proteinuria. Abnormal placentation associated with shallow trophoblast invasion (fetal cells from outer cell layer of the blastocyst) into endometrium (decidua) and improper spiral artery remodeling in the decidua are initial pathological steps. In this study we analyzed the renin-angiotensin system in adipose tissue, decidua and placenta from women with uneventful pregnancy and women with preeclampsia. We also analyzed the tissue by Affymetrix chips in a comparison study (control vs. preeclampsia) Keywords: disease comparison, disease state
2007-01-01 | GSE6573 | GEO
Project description:Background: Early-onset preeclampsia (EOPE) and late-onset preeclampsia (LOPE) has been regarded as two different phenotypes with heterogeneous manifestation. The underlying mechanisms remain elusive. Aim to gain insight into the pathogenesis of the two traits, we analyzed the placental gene expression profiles in preeclampsia placentas. Methods: Whole genome-wide microarray was used to describe the gene expression profiles in the placenta tissues from patients with early-(n=7; <34 weeks), late-onset(n=8; >36 weeks) PE and their controls who delivered preterm (n=5;<34 weeks) or at term(n=5; >36 weeks) Genes were selected as differentially expressed upon a fold-changeâ?¥2 and q-value<0.05. qRT-PCR was undertaken to verify the results. Western blot was further performed to verify secreted genes at the protein level. Results: A total of 627 genes were differentially expressed in early-compared with late-onset PE. Of these, 177 genes were up-regulated and 450 genes down-regulated in early-onset PE. Go analysis showed significant alteration in several biological processes, in addition to the processes which have been found before, such as immune and inflammatory response, cell adhension, female pregnancy and blood vessel development. We also found alteration in G-protein coupled receptor protein signaling pathway, G protein-coupled receptor 124 (GPR124) (P=0.0064) and MAS-related GPR, member F (MRGPRF)(P=0.0155 ) were both down-regulated obviously in early-onset PE. Conclusion: The different gene expression profiles suggested early- and late-onset PE are separate disease entities. Moreover, G-protein coupled receptor protein signaling pathway may contribute to the mechanism underlying early- and late-onset preeclampsia. Whole genome-wide microarray was used to describe the gene expression profiles in the placenta tissues from patients with early-(n=7; <34 weeks), late-onset (n=8; >36 weeks) PE and their controls who delivered preterm(n=5;<34 weeks) or at term(n=5; >36 weeks). Pooled controls who delivered at term were labled with cy5.
2015-10-27 | E-GEOD-74341 | biostudies-arrayexpress
Project description:Preeclampsia (PE) is a pregnancy disorder characterized by high blood pressure and proteinuria that can cause adverse health effects in both mother and fetus. There is no current cure for PE other than delivery of the fetus. While the etiology is unknown, poor placentation of the placenta due to aberrant signaling of growth and angiogenic factors has been postulated as causal factors of PE. In addition, environmental contaminants, such as the metal cadmium (Cd), have been linked to placental toxicity and increased risk of developing PE. Here, we use a translational study design to investigate genomic and epigenomic alterations in both placentas and placental trophoblasts, focused on the angiogenesis-associated transforming growth factor-beta (TGF-β) pathway. Genes within the TGF-β pathway displayed increased expression in both the preeclamptic placenta and Cd-treated trophoblasts. In addition, miRNAs that target the TGF-β pathway were also significantly altered within the preeclamptic placenta and Cd-treated trophoblasts. Integrative analysis resulted in the identification of a subset of Cd-responsive miRNAs, including miR-26a and miR-155, common to preeclamptic placentas and Cd-treated trophoblasts. These miRNAs have previously been linked to PE and are predicted to regulate members of the TGF-β pathway. Results from this study provide future targets for PE treatment.
2016-07-12 | GSE84260 | GEO
Project description:Preeclampsia (PE) is a serious pregnancy associated disorder. Recently, it has been proposed that the role of the placenta differ between the two sub-groups early- and late-onset PE. To further elucidate differences between the two sub-groups, we conducted transcriptional profiling of human placenta comparing early- with late-onset PE. The analysis showed differences in angiogenesis associated genes. Two-condition experiment, early-onset PE (n=8) vs. late-onset PE (n=7).
2011-02-28 | E-GEOD-22526 | biostudies-arrayexpress