Influence of plasma from normal and preeclamptic women on HUVEC cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Daniel Vaiman
PROVIDER: E-GEOD-41681 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Plasma from normal and preeclamptic pregnancies was collected and added in the culture medium of HUVEC cells. The aims are double: identifying putative biomarkers that could be modified recurrently in the endothelium under preeclampsia and understand at term the molecular bases of the increased risk of cardiovascular and kidney diseases in woman that have had a preeclampsia.
2013-06-30 | GSE41681 | GEO
Project description:Plasma from pregnant women were applied three days in three steps to HUVEC cells. RNAs were isolated and prepared. Four pools of RNAs were obtained, two of them from cells exposed to preeclamptic plasma (2 and 3, corresponding to mild and severe preeclampsia, respectively) and two from cells exposed to normal plasma from pregnant women (five and five).
2015-06-29 | E-MTAB-3348 | biostudies-arrayexpress
Project description:Preeclampsia (PE) is a major contributor of maternal mortality with uncertain etiology. Recent studies suggested that epigenetic modifications, including DNA methylation, play a vital role in the development of PE. In this study, we have mapped genome-wide distribution of 5-methylcytosin (5-mC) and 5-hydroxymethylcytosine (5-hmC) using MeDIP and (h)MeDIP in the placentas from severely preeclamptic patients and normal controls. A total 194485 pooled 5-mC peaks and 138133 pooled 5-hmC peaks were identified, of which 714 5-mC peaks and 119 5-hmC peaks showed significant difference between patients and controls (>2-fold, p<0.05).To our knowledge, this is the first report of DHMRs (Differentially Hydroxy-Methylated Regions) in preeclamptic placenta. We not only confirmed the aberrant DNA methylated regions in the process of preeclampsia reported previously, but also identified unreported regions. A total of 4 selected DMRs (Differentially Methylated Regions) were also confirmed by MassARRAY EppiTYPER. Of these, PTPRN2, which had low level of 5-mC and high level of 5-hmC at gene body, was further verified to have lower methylation level at promoter regions in case group compared with controls. In conclusion, our study provided genome-wide distribution of 5-mC and 5-hmC in severe PE and normal controls, which have further clinical value for the identification of diagnostic and therapeutic markers for severe PE. Examination of 5-mC and 5-hmC pattern in 4 control cases' tissue and 4 severely Preeclamptic Placentas cases' tissue.
2014-12-13 | E-GEOD-63743 | biostudies-arrayexpress
Project description:Prenatal development is a critical period for programming of neurological disease. Preeclampsia, a pregnancy complication involving oxidative stress in the placenta, has been associated with long-term health implications for the child, including an increased risk of developing schizophrenia and autism spectrum disorders in later life. We have shown previously, in a rodent model of placental oxidative stress, that culture medium conditioned by the placenta alters neuronal characteristics when applied to primary cortical cultures in vitro and mimics many of the neurodevelopmental changes observed in the offspring brain. To further investigate if molecules released by the placenta may be important mediators in foetal programming of the brain, we analysed if placental tissue delivered from patients with preeclampsia secreted molecules that could affect cortical cells in culture. Application of culture medium conditioned by preeclamptic placentae to mixed cortical cultures caused changes in neurons and astrocytes that were related to key changes observed in brains of patients with schizophrenia and autism, including effects on dendrite lengths, astrocyte number as well as glutamate and GABA receptors. Treatment of the placental explants with an antioxidant prevented neuronal abnormalities. Furthermore, we identified that bidirectional communication between neurons and astrocytes, potentially via glutamate, is required to produce the effects of preeclamptic placenta medium on cortical cells. Analysis of possible signalling molecules in the placenta conditioned medium showed that the secretion profile of extracellular microRNA, small posttranscriptional regulators, was altered in preeclampsia and partially rescued by antioxidant treatment of the placental explants. Predicted targets of these differentially abundant microRNAs were linked to neurodevelopment and the placenta. The presented study provides further evidence that the diseased placenta may release factors that damage cortical cells in the brain and suggests the possibility of targeted antioxidant treatment of the placenta to prevent neurodevelopmental disorders.
2019-02-11 | GSE110786 | GEO
Project description:Background Mutations in STOX1 were proposed as causal for predisposing to preeclampsia, a hypertensive disorder originating from placental defects, affecting up to 10% of human pregnancies. However, after the first study published in 2005 three other groups have dismissed the polymorphism described in the first paper as a causal mutation. Methodology and Principal Findings In the present study, we have developed a choriocarcinoma cell line overexpressing STOX1. This overexpression results in the transcriptional modification of 12.5% of the genes, some of them being direct targets as shown by chromatin immunoprecipitation. STOX1 overexpression correlates strongly and specifically with transcriptomic alterations in preeclamptic placentas (r=0.30, p=9.10-7). Numerous known key modulators of preeclampsia (such as Endoglin, Syncytin, human chrionic gonadotrophin-hCG-, and Glial Cell Missing Homolog -GCM1-) were modified in these transformed choriocarcinoma cells. Conclusions Our results contribute to reconcile contradictory data about the involvement of STOX1 in preeclampsia. In addition, they strongly suggest that anomalies in STOX1 expression are associated with the onset of preeclampsia, thus indicating that this gene should be the target of future studies. Furthermore, our cellular model could constitute an invaluable resource for studying specific aspects of this human disease.
2008-11-07 | GSE13475 | GEO
Project description:Background; Mutations in STOX1 were proposed as causal for predisposing to preeclampsia, a hypertensive disorder originating from placental defects, affecting up to 10% of human pregnancies. However, after the first study published in 2005 three other groups have dismissed the polymorphism described in the first paper as a causal mutation. Methodology and Principal Findings; In the present study, we have developed a choriocarcinoma cell line overexpressing STOX1. This overexpression results in the transcriptional modification of 12.5% of the genes, some of them being direct targets as shown by chromatin immunoprecipitation. STOX1 overexpression correlates strongly and specifically with transcriptomic alterations in preeclamptic placentas (r=0.30, p=9.10-7). Numerous known key modulators of preeclampsia (such as Endoglin, Syncytin, human chrionic gonadotrophin-hCG-, and Glial Cell Missing Homolog -GCM1-) were modified in these transformed choriocarcinoma cells. Conclusions; Our results contribute to reconcile contradictory data about the involvement of STOX1 in preeclampsia. In addition, they strongly suggest that anomalies in STOX1 expression are associated with the onset of preeclampsia, thus indicating that this gene should be the target of future studies. Furthermore, our cellular model could constitute an invaluable resource for studying specific aspects of this human disease. Experiment Overall Design: Microarrays expression
2008-11-14 | E-GEOD-13475 | biostudies-arrayexpress
Project description:Preeclampsia (PE) is a major contributor of maternal mortality with uncertain etiology. Recent studies suggested that epigenetic modifications, including DNA methylation, play a vital role in the development of PE. In this study, we have mapped genome-wide distribution of 5-methylcytosin (5-mC) and 5-hydroxymethylcytosine (5-hmC) using MeDIP and (h)MeDIP in the placentas from severely preeclamptic patients and normal controls. A total 194485 pooled 5-mC peaks and 138133 pooled 5-hmC peaks were identified, of which 714 5-mC peaks and 119 5-hmC peaks showed significant difference between patients and controls (>2-fold, p<0.05).To our knowledge, this is the first report of DHMRs (Differentially Hydroxy-Methylated Regions) in preeclamptic placenta. We not only confirmed the aberrant DNA methylated regions in the process of preeclampsia reported previously, but also identified unreported regions. A total of 4 selected DMRs (Differentially Methylated Regions) were also confirmed by MassARRAY EppiTYPER. Of these, PTPRN2, which had low level of 5-mC and high level of 5-hmC at gene body, was further verified to have lower methylation level at promoter regions in case group compared with controls. In conclusion, our study provided genome-wide distribution of 5-mC and 5-hmC in severe PE and normal controls, which have further clinical value for the identification of diagnostic and therapeutic markers for severe PE.
2014-12-13 | GSE63743 | GEO
Project description:The purpose of this study was to determine the difference of the miRNA profiles between normal and preeclamptic placenta.
2014-04-25 | GSE57050 | GEO
Project description:The purpose of this study was to determine the difference of the miRNA profiles between normal and preeclamptic placenta. Ten placental samples were analyzed. Six were from preeclamptic patients and four were from normal pregnancies.
2014-04-25 | E-GEOD-57050 | biostudies-arrayexpress
Project description:Long-term consequences of preeclampsia were studied by high-throughput approaches (Transcriptomics, Luminex cytokine profile) in mice 8 months after the disease in the heart, in the endothelial cells and in the plasma. In the heart we found a persisting ventricular hypertrophy with an altered histology and an abnormal ultrasound Doppler profile under effort simulation by dobutamine injection. The transcriptomic profile of the endothelium revealed a deregulation for 1149 genes (327 down-regulated and 822 up-regulated, with a threshold of 1.5, p<0.05). The up-regulated genes could be grouped consistently in gene pathways and gene ontology terms mainly focused on Inflammation and Stress sensu lato. A cytokine profile of the mouse serum was carried out. Using a combination of 8 cytokines (Cxcl13, Cxcl16, Cxcl11, Il-16, Il-10, Il-2, Il-4 and Ccl1) in a Discriminant Analysis, we were able to separate unambiguously the mice having had a preeclamptic pregnancy from the controls. Seven out of eight of these cytokines (with the exception of Il-16) varied in the same direction in the endothelium and in the plasma. In sum, our study shows that preeclampsia alone is able to trigger considerable long-term consequences, and suggests that specific cytokines could help to improve the follow-up of patients long after a preeclamptic pregnancy.
2019-06-01 | E-MTAB-7358 | biostudies-arrayexpress