Treating the placenta to prevent adverse effects of gestational hypoxia on fetal brain development
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA341704 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4125040_1.fastq.gz | Fastqsanger.gz | |||
| SRR4125040_2.fastq.gz | Fastqsanger.gz | |||
| SRR4125050_1.fastq.gz | Fastqsanger.gz | |||
| SRR4125050_2.fastq.gz | Fastqsanger.gz | |||
| SRR4125060_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 64 |
Similar Datasets
Project description:Some neuropsychiatric disease, including schizophrenia, may originate during prenatal development, following periods of gestational hypoxia and placental oxidative stress. Here we investigated if gestational hypoxia promotes damaging secretions from the placenta that affect fetal development and whether a mitochondria-targeted antioxidant MitoQ might prevent this. Gestational hypoxia caused low birth-weight and changes in young adult offspring brain, mimicking those in human neuropsychiatric disease. Exposure of cultured neurons to fetal plasma or to secretions from the placenta or from model trophoblast barriers that had been exposed to altered oxygenation caused similar morphological changes. The secretions and plasma contained altered microRNAs whose targets were linked with changes in gene expression in the fetal brain and with human schizophrenia loci. Molecular and morphological changes in vivo and in vitro were prevented by a single dose of MitoQ bound to nanoparticles, which were shown to localise and prevent oxidative stress in the placenta but not in the fetus. We suggest the possibility of developing preventative treatments that target the placenta and not the fetus to reduce risk of psychiatric disease in later life.
2017-08-22 | GSE86346 | GEO
Project description:Some neuropsychiatric disease, including schizophrenia, may originate during prenatal development, following periods of gestational hypoxia and placental oxidative stress. Here we investigated if gestational hypoxia promotes damaging secretions from the placenta that affect fetal development and whether a mitochondria-targeted antioxidant MitoQ might prevent this. Gestational hypoxia caused low birth-weight and changes in young adult offspring brain, mimicking those in human neuropsychiatric disease. Exposure of cultured neurons to fetal plasma or to secretions from the placenta or from model trophoblast barriers that had been exposed to altered oxygenation caused similar morphological changes. The secretions and plasma contained altered microRNAs whose targets were linked with changes in gene expression in the fetal brain and with human schizophrenia loci. Molecular and morphological changes in vivo and in vitro were prevented by a single dose of MitoQ bound to nanoparticles, which were shown to localise and prevent oxidative stress in the placenta but not in the fetus. We suggest the possibility of developing preventative treatments that target the placenta and not the fetus to reduce risk of psychiatric disease in later life.
2017-08-22 | GSE86408 | GEO
Project description:Hypoxia-related pregnancy complications increase the risk of disease in the child in later life. No prevention is available. Previously we noted that a trophoblast barrier, an in vitro model of the placenta, reacted to oxidative stress by secreting factors that damage neighbouring cells. Application of mitochondrion-targeted antioxidant MitoQ prevented this. Here we tested the effects of MitoQ-bound nanoparticles on trophoblast barriers and in a rat model of gestational hypoxia.A single dose of MitoQ-nanoparticles, administered maternally before a hypoxic episode, reduced oxidative stress in the placental barrier without reaching the fetus and prevented changes to birthweight. MitoQ-nanoparticles further suppressed damaging signalling from the placental barriers. Altered signalling molecules in the fetal plasma and in conditioned media from rat placenta included changes to proteins with relevance to cardiovascular disease. We suggest as a future possibility, treatment of the placenta to prevent disease in the offspring in later life.
2017-08-22 | PXD004955 | Pride
Project description:Hypoxia-related pregnancy complications increase the risk of disease in the child in later life. No prevention is available. Previously we noted that a trophoblast barrier, an in vitro model of the placenta, reacted to oxidative stress by secreting factors that damage neighbouring cells. Application of mitochondrion-targeted antioxidant MitoQ prevented this. Here we tested the effects of MitoQ-bound nanoparticles on trophoblast barriers and in a rat model of gestational hypoxia.A single dose of MitoQ-nanoparticles, administered maternally before a hypoxic episode, reduced oxidative stress in the placental barrier without reaching the fetus and prevented changes to birthweight. MitoQ-nanoparticles further suppressed damaging signalling from the placental barriers. Altered signalling molecules in the fetal plasma and in conditioned media from rat placenta included changes to proteins with relevance to cardiovascular disease. We suggest as a future possibility, treatment of the placenta to prevent disease in the offspring in later life.
2017-08-22 | PXD004956 | Pride
Project description:This SuperSeries is composed of the SubSeries listed below.
2017-08-22 | GSE86410 | GEO
Project description:Some neuropsychiatric disease, including schizophrenia, may originate during prenatal development, following periods of gestational hypoxia and placental oxidative stress. Here we investigated if gestational hypoxia promotes damaging secretions from the placenta that affect fetal development and whether a mitochondria-targeted antioxidant MitoQ might prevent this. Gestational hypoxia caused low birth-weight and changes in young adult offspring brain, mimicking those in human neuropsychiatric disease. Exposure of cultured neurons to fetal plasma or to secretions from the placenta or from model trophoblast barriers that had been exposed to altered oxygenation caused similar morphological changes. The secretions and plasma contained altered microRNAs whose targets were linked with changes in gene expression in the fetal brain and with human schizophrenia loci. Molecular and morphological changes in vivo and in vitro were prevented by a single dose of MitoQ bound to nanoparticles, which were shown to localise and prevent oxidative stress in the placenta but not in the fetus. We suggest the possibility of developing preventative treatments that target the placenta and not the fetus to reduce risk of psychiatric disease in later life.
| S-EPMC5567270 | biostudies-literature
Project description:Affymetrix miRNA arrays were used to generate miRNA profiles in placenta of Meishan and Yorkshire pigs on stages of initiation (gestational day 26) and establishment (gestational day 50) of placental folds development. The study allowed for the determination of the miRNAs that were differentially expressed in porcine placenta on different gestational day. This study will provide the information to better understanding of the role miRNAs in porcine placental development.
2015-10-01 | GSE62996 | GEO
Project description:Treating the placenta to prevent adverse effects of gestational hypoxia on fetal brain development [RNAseq]
| PRJNA341706 | ENA
Project description:Treating the placenta to prevent adverse effects of gestational hypoxia on fetal brain development [microRNA]
| PRJNA341488 | ENA
Project description:Data on the temporal dynamics of human placental gene expression is scarce. We have completed the first whole-genome profiling of human placental gene expression dynamics (GeneChips, Affymetrix®) from early to mid- gestation (10 samples; gestational weeks 5 to 18) and report 154 genes with considerable change in transcript levels (FDR P<0.1). Functional enrichment analysis revealed >200 GO categories that are statistically over-represented among 105 genes with dynamically increasing transcript levels. Analysis in an extended sample (n=43; gestational weeks 5 to 41) conformed a highly significant (FDR P<0.05) expressional peak in mid-gestation placenta for ten genes: BMP5, CCNG2, CDH11, FST, GATM, GPR183, ITGBL1, PLAGL1, SLC16A10, STC1. A central hypothesis of our study states that the aberrant expression of genes characteristic to mid-gestation placenta may contribute to affected fetal growth, maternal preeclampsia (PE) or gestational diabetes (GD). The gene STC1 coding for Stanniocalcin 1 (STC1) was identified with a sharp placental expressional peak in mid-gestation, increased mRNA levels at term and significantly elevated STC1 protein levels in post-partum maternal plasma in all pregnancy complications. The highest STC1 levels were identified in women, who developed simultaneously PE and delivered an SGA baby (median 731 vs 418 pg/ml in controls; P=0.001). CCNG2 and LYPD6 exhibited significantly increased placental mRNA expression and enhanced intensity of immunohistochemistry staining in placental sections all studied in GD and PE cases. Aberrant expression of mid-gestation specific genes in pregnancy complications at term indicates the importance of the fine-scale tuning of the temporal dynamics of transcription regulation in placenta. Observed significantly elevated plasma STC1 in complicated pregnancies warrants further investigations of its potential as a biomarker. Interestingly, a majority of genes with high expression in mid-gestation placenta have also been implicated in adult complex disease. This observation promotes a recently opened discussion on the role of placenta in developmental programming. 4 samples; this submission is extension of our earlier study (accession GSE22490).
2012-05-10 | E-GEOD-37901 | biostudies-arrayexpress