Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA341706 | 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 |
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Project description:Treating the placenta to prevent adverse effects of gestational hypoxia on fetal brain development [microRNA]
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Project description:Treating the placenta to prevent adverse effects of gestational hypoxia on fetal brain development
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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 | PXD004956 | 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 | PXD004955 | Pride
Project description:<p>Over 135 million births occur each year; yet, the molecular underpinnings of human parturition in gestational tissues, and in particular the placenta, are still poorly understood. The placenta is a complex heterogeneous organ including cells of both maternal and fetal origin, and insults that disrupt the maternal-fetal dialogue could result in adverse pregnancy outcomes such as preterm birth. There is limited knowledge of the cell type composition and transcriptional activity of the placenta and its compartments during physiologic and pathologic parturition. To fill this knowledge gap, we used scRNA-seq to profile the placental villous tree, basal plate, and chorioamniotic membranes of women with or without labor at term and those with preterm labor. </p>
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Project description:Gestational diabetes (GDM) refers to diabetes diagnosed as diabetes in the second or third trimester of pregnancy, but not obvious before pregnancy. It is one of the most common complications of pregnancy, which can lead to perinatal asphyxia, neonatal hypoglycemia, macrosomia, cardiovascular abnormalities, obesity and other short-term and long-term adverse outcomes of the offspring. This study explores the differential expression of transcriptome between GDM and non GDM placenta, and explores the impact of subtle metabolic changes in the placenta on fetal growth and development during GDM in pregnant women.
2024-07-30 | GSE263483 | GEO
Project description:The placenta regulates maternal-fetal communication, and its defect leads to significant pregnancy complications. The maternal and embryonic circulations are primitively connected in early placentation, but the function of the placenta during this developmentally essential period is relatively unknown. We thus performed a comparative proteomic analysis of the placenta before and after primary placentation and found that the metabolism and transport of lipids were characteristically activated in this period. The placental fatty acid (FA) carriers in specific placental compartments were upregulated according to gestational age, and metabolomic analysis also showed that the placental transport of FAs increased in a time-dependent manner. Further analysis of two mutant mice models with embryonic lethality revealed that lipid-related signatures could reflect the functional state of the placenta. Our findings highlight the importance of the nutrient transport function of the primary placenta in the early gestational period and the role of lipids in embryonic development.
2023-09-06 | PXD026858 | Pride
Project description:Few studies have assessed the patterns of parasite populations of rodents over a longitudinal gradient in Chile. In this work, the gastrointestinal helminthic fauna of invasive rodents in Chile was examined to assess the association between their presence/absence and abundance with latitude, host sex, and host body condition, and to assess the coexistence and correlation of the abundance between parasite species. Rodents were obtained from 20 localities between 33 and 43°S. Helminths were extracted from the gastrointestinal tract and identified morphologically. Overall, 13 helminth taxa were obtained. The most frequently identified parasite species was Heterakis spumosa, and the most abundant was Syphacia muris, while Physaloptera sp. was the most widely distributed. No locality presented with a coexistence that was different from that expected by chance, while the abundance of five helminthic species correlated with the abundance of another in at least one locality, most likely due to co-infection rather than interaction. Host sex was associated with parasite presence or abundance, and female sex-biased parasitism was notably observed in all cases. Body condition and latitude presented either a positive or negative association with the presence or abundance of parasites depending on the species. It is notable that the likely native Physaloptera sp. is widely distributed among invasive rodents. Further, gravid females were found, suggesting spillback of this species to the native fauna. The low frequency and abundance of highly zoonotic hymenolepid species suggest that rodents are of low concern regarding gastrointestinal zoonotic helminths.
| S-EPMC9277659 | biostudies-literature