Prenatal screening for miRNAs in fetal diseases
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ABSTRACT:
PROVIDER: PRJNA1013352 | ENA |
REPOSITORIES: ENA
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Project description:Distinct miRNA expression patterns may reflect anomalies related to fetal malformations such as spinal bifida (SB) or congenital diaphragmatic hernia (CDH), which could shed light on novel pathomechanism determination and subsequent diagnostic significance evaluation. The aim of this study was to determine the miRNA maternal expression profile in plasma and amniotic fluid samples of women carrying fetuses with SB and CDH.
2024-03-20 | GSE242364 | GEO
Project description:The Ts1Cje mouse strain (Sago, 1998) contains a segmental trisomy of mouse chromosome 16 orthologous to the region of human chromosome 21 commonly associated with Down Syndrome. In this study, fetuses were obtained from wildtype mothers bred with either wildtype or Ts1Cje males. Gene expression profiles in fetal liver and placenta of wildtype and Ts1Cje fetuses were compared, to identify potential markers for application in human prenatal DS screening. A 48 array study with 24 arrays for placenta and 24 for fetal liver. For each tissue we used RNA from 24 individual embryos, i.e. six male and six female embryos from both genotypes.
2011-05-11 | E-GEOD-24272 | biostudies-arrayexpress
Project description:The Ts1Cje mouse strain (Sago, 1998) contains a segmental trisomy of mouse chromosome 16 orthologous to the region of human chromosome 21 commonly associated with Down Syndrome. In this study, fetuses were obtained from wildtype mothers bred with either wildtype or Ts1Cje males. Gene expression profiles in fetal liver and placenta of wildtype and Ts1Cje fetuses were compared, to identify potential markers for application in human prenatal DS screening.
2011-05-11 | GSE24272 | GEO
Project description:Prenatal stress is one of the risk factors for the development of mental disorders in offspring, but its underlying mechanism remains elusive. To perform epigenomic profiling of prenatal stress effects on fetal brains, ATAC-seq and RNA-seq were used to explore the changes of chromatin accessibility and gene expression on embryonic brains at E15.5 of offspring from pregnant mice, which were exposed to chronic mild unpredictable stress between E5.5 to E14.5.
2023-03-01 | GSE205087 | GEO
Project description:Isolation of tissue-specific fetal stem cells and derivation of primary organoids is currently limited to post-termination samples. This hampers the prenatal investigation of fetal development and congenital diseases. Therefore, novel patient-specific in vitro models are needed. To this aim, isolation and expansion of fetal stem cells during pregnancy, without the need for tissue or cellular reprogramming, would be advantageous. The amniotic fluid (AF) is a source of cells originating from multiple developing organs. Using single cell analysis, we characterised the cellular identities present in the human AF. We identified and isolated viable epithelial stem/progenitor cells of fetal gastrointestinal, renal and pulmonary origin. Upon culture, these cells formed clonal epithelial organoids, manifesting small intestine, kidney tubule and lung identity. AF organoids (AFO) exhibit transcriptomic, protein expression and functional features of their tissue of origin. With relevance for prenatal disease modelling, we derived lung organoids from the amniotic and tracheal fluid cells of Congenital Diaphragmatic Hernia (CDH) fetuses. CDH organoids show differences to non-CDH controls recapitulating some features of the disease. AFO are derived in a timeline compatible with prenatal intervention, potentially allowing investigation of therapeutic tools and regenerative medicine strategies personalised to the fetus at clinically relevant developmental stages.
2023-12-15 | GSE220994 | GEO
Project description:Epigenomic profiling in fetal brain after prenatal stress
| PRJNA843693 | ENA
Project description:Cannabis use during pregnancy is associated with adverse neurodevelopmental outcomes. However, the underlying mechanisms and effects of cannabis on fetal development are relatively unknown. We determined the impact of chronic delta-9-tetrahydrocannabinol (THC, cannabis’s main psychoactive component) exposure on fetal development in a rhesus macaque model using advanced imaging combined with molecular and tissue studies. Animals were divided into control (n=5) or THC-exposed (n=5) groups, which received a daily THC edible pre-conception and throughout pregnancy. Animals underwent fetal brain T2-weighted MRI at gestational days 85 (G85), G110, G135 and G155 (term is ~G168) to assess brain development. All animals underwent cesarean delivery with fetal cerebral spinal fluid (CSF) and brain collection at G155 for microRNA (miRNA) and histologic analysis. THC exposure did not demonstrate any fetal brain volumetric changes. However, histological findings in THC-exposed brains suggested brain dysregulation that may have long-term developmental implications. We identified two extracellular-vesicle-associated miRNAs (mir-448 and mir-199a-3p) with>2-fold change in CSF with maternal THC use. Amniotic fluid (AF) was collected at the 4 gestational ages (GA) and relative protein abundance changes measured with isobaric labeling quantitative proteomics. Changes in AF were observed across the GAs and in response to THC-treatment.
2025-07-18 | PXD042447 | Pride
Project description:Development of a common platform for the noninvasive prenatal diagnosis of X-linked diseases
| PRJEB26532 | ENA
Project description:Prenatal maternal stress (PNMS) determines lifetime mental and physical health. Here, we show in rats that PNMS has consequences for placental function and fetal brain development across four generations (F0-F3). Using a systems biology approach, comprehensive DNA methylation (DNAm), miRNA, and mRNA profiling revealed a moderate impact of PNMS in the F1 generation, but drastic changes in F2 and F3 generations, suggesting compounding effects of PNMS with each successive generation. Both maternal and placental miRNA gene targets included de novo DNA methyltransferases, indicating robust PNMS-induced disruption in the complex epigenetic regulatory network between miRNAs and DNAm. Transgenerational programming mainly involved genes and biological pathways associated with neurological and psychiatric diseases which were linked to maternal-fetal crosstalk facilitated by the placenta. The highly correlated placenta-brain profiles support the use of placenta as a noninvasive biomarker resource to predict pathological changes in the neonatal brain. The transgenerational persistence of critical DNAm, miRNA and mRNA signatures may explain familial non-genetic disease risks.
2024-10-07 | GSE276382 | GEO
Project description:Prenatal maternal stress (PNMS) determines lifetime mental and physical health. Here, we show in rats that PNMS has consequences for placental function and fetal brain development across four generations (F0-F3). Using a systems biology approach, comprehensive DNA methylation (DNAm), miRNA, and mRNA profiling revealed a moderate impact of PNMS in the F1 generation, but drastic changes in F2 and F3 generations, suggesting compounding effects of PNMS with each successive generation. Both maternal and placental miRNA gene targets included de novo DNA methyltransferases, indicating robust PNMS-induced disruption in the complex epigenetic regulatory network between miRNAs and DNAm. Transgenerational programming mainly involved genes and biological pathways associated with neurological and psychiatric diseases which were linked to maternal-fetal crosstalk facilitated by the placenta. The highly correlated placenta-brain profiles support the use of placenta as a noninvasive biomarker resource to predict pathological changes in the neonatal brain. The transgenerational persistence of critical DNAm, miRNA and mRNA signatures may explain familial non-genetic disease risks.
2024-10-07 | GSE276226 | GEO