Gene expression changes in cerebellar meninges in Pdgfc and Pdgfra mutant mice at P0
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus Mus
PROVIDER: GSE202835 | GEO | 2022/07/28
REPOSITORIES: GEO
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Project description:Platelet-derived growth factor-C (PDGF-C) is one of three known ligands for the tyrosine kinase receptor PDGFRα. Analysis of Pdgfc null mice has demonstrated roles for PDGF-C in palate closure and the formation of cerebral ventricles, but redundancy with other PDGFRα ligands might hide additional functions. In search of further developmental roles for PDGF-C, we generated mice that were double mutants for Pdgfc -/- and Pdgfra GFP/+. These mice display a range of severe phenotypes including cerebellar malformation, neuronal over-migration in the cerebral cortex, spina bifida and lung emphysema. We focused our analysis on the central nervous system (CNS), where PDGF-C was identified as a critical factor for the formation of meninges and assembly of the glia limitans basement membrane.
2016-02-24 | GSE67644 | GEO
Project description:Platelet-derived growth factor-C (PDGF-C) is one of three known ligands for the tyrosine kinase receptor PDGFRα. Analysis of Pdgfc null mice has demonstrated roles for PDGF-C in palate closure and the formation of cerebral ventricles, but redundancy with other PDGFRα ligands might hide additional functions. In search of further developmental roles for PDGF-C, we generated mice that were double mutants for Pdgfc -/- and Pdgfra GFP/+. These mice display a range of severe phenotypes including cerebellar malformation, neuronal over-migration in the cerebral cortex, spina bifida and lung emphysema. We focused our analysis on the central nervous system (CNS), where PDGF-C was identified as a critical factor for the formation of meninges and assembly of the glia limitans basement membrane. Meninges freely dissected and released from P0 cerebrum. RNA was isolated using RNeasy micro kit (Qiagen) and quality checked in a 2100 BioAnalyzer (Agilent Technologies, Santa Clara, CA, USA). Transcription profiling was performed with Gene Chip Mouse Gene 1.0 ST array. We compared Pdgfc-/-; Pdgfra GFP/+ mice, with a control group consisting of all littermates (Pdgfc+/+, Pdgfc+/-, Pdgfc-/-, Pdgfc+/+; Pdgfra GFP/+ and Pdgfc+/-; Pdgfra GFP/+). One litter was used, including 4 mutants and 9 controls
2016-02-24 | E-GEOD-67644 | biostudies-arrayexpress
Project description:Platelet-derived growth factor-C (PDGF-C) is one of three known ligands for the tyrosine kinase receptor PDGFR-alpha. Analysis of Pdgfc null mice has demonstrated roles for PDGF-C in palate closure and the formation of cerebral ventricles, but redundancy with other PDGFR-alpha ligands might hide additional functions. In search of further developmental roles for PDGF-C, we generated mice that were double mutants for Pdgfc -/- and Pdgfra GFP/+. These mice display a range of severe phenotypes including cerebellar malformation, neuronal over-migration in the cerebral cortex, spina bifida and lung emphysema. We focused our analysis on the central nervous system (CNS), where PDGF-C was identified as a critical factor for the formation of meninges and assembly of the glia limitans basement membrane.
2022-07-28 | GSE77049 | GEO
Project description:Fetal spina bifida can associate with reduced fetal growth. However, little is known about placental development and function in pregnancies with fetal spina bifida, despite that the placenta is a critical regulator of fetal growth. We used data from a case-control study to determine how the placental transcriptome differs in fetuses with isolated spina bifida (cases), compared to fetuses without any congenital anomalies (controls).
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Project description:Intraventricular hemorrhage (IVH) is a significant complication of premature infants. With improved preterm infant survival, there is increased incidence of severe IVH, and the potential for lifelong neurodevelopmental deficits. Neurological complications are high in babies that develop hydrocephalus as a result of IVH and require a permanent ventriculoperitoneal (VP) shunt. Spina bifida is a congenital disorder caused by the incomplete closure of the neural tube. Hydrocephalus is also a common complication of spina bifida, presenting in 15 to 25% of cases. Often, when spina bifida is identified and surgically repaired, CSF shunting mechanisms are placed in a high percentage of cases. A better understanding of the events leading to the development of hydrocephalus will help clinicians make more informed decisions about the need for CSF shunting and other interventions. Extracellular RNAs (exRNAs) may be indicators of the multiple pathological events surrounding the development of hydrocephalus in subjects with intraventricular hemorrhage or spina bifida. exRNAs may also be indicators for the presence and magnitude of neurodevelopmental outcomes. Under that premise, we sequenced the total exRNA in CSF from children that had IVH or spina bifida, some of which developed hydrocephalus and/or had reported developmental delays.
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Project description:Neural tube closure in vertebrates is achieved through a highly dynamic and coordinated series of morphogenic events involving neural plate, surface ectoderm, and neural plate border. Failure of this process in the caudal region causes spina bifida. Grainyhead-like 3 (GRHL3) is an indispensable transcription factor for neural tube closure as constitutive inactivation of which leads to fully penetrant spina bifida. Here, through single-cell transcriptomics we show that at E8.5, the time-point preceding mouse neural tube closure, the co-expression of Grhl3, Tfap2a, and Tfap2c defines a previously unrecognised progenitor population of surface ectoderm. Specific deletion of Grhl3 expression using Tfap2a-Cre recapitulate the spina bifida observed in Grhl3-null animals. Moreover, conditional inactivation of Tfap2c expression in Grhl3-expressing neural plate border cells also causes mild spina bifida. These findings clearly indicate that Grhl3-expressing neural plate border cells cohort is required for the early-stage neurulation.
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Project description:Background The vitamin A derivative, retinoic acid (RA), is a potent teratogenic agent that induces a variety of congenital abnormalities including neural tube defects. The embryopathology of RA has been extensively investigated and retinol receptors play important roles during organogenesis, development and neural tube closure. Still, the mechanisms by which RA influences these processes are not completely understood. Methods We used a custom-made mouse genome 32K oligonucleotide microarray to determine the gene expression profiles of mouse embryo spinal cord samples that had been exposed to vehicle or RA. Then, we performed a GSEA (gene set enrichment analysis) on the gene expression data by searching MSigDB (v2.5) c2 gene sets (canonical pathways) and c5 gene sets (curated GO terms), with set size restraints on the range to avoid over-narrow or over-broad categories. Results Using microarray technology, the present study identifies 85 genes in the spinal cord that exhibit at least a 1.5-fold change between control samples and samples with spina bifida aperta. A gene set enrichment analysis showed that maternal exposure to RA induced spinal bifida that were associated with altered expression of genes involved in pro- or anti-apoptosis, cell proliferation, migration, cytoskeleton components, and cell or focal adhesion, indicating that defective functions of these cell components and biological processes preceded the abnormal development of neural tube. Conclusions Maternal exposure to RA induced spinal bifida that were associated with altered expression of genes involved in pro- or anti-apoptosis, cell proliferation, migration, cytoskeleton components, and cell or focal adhesion. As shown in previous reports, defective functions of these cell components and biological processes preceded the abnormal development of the neural tube. Our study will help the understanding of the etiology and pathology of spinal bifida. However, it should be noted that the changes in gene expression induced by RA exposure may not be an effect on events other than neural tube closure; further study is required to fully understand the molecular mechanisms and consequence of neural tube defects in embryos exposed to RA. Our study provides a global analysis of gene expression patterns in spina bifida and will help the understanding of the etiology and pathology of neural tube defects. We assessed the changes in gene expression that coincide with spina bifida in RA-treated mouse fetuses. After generating an independent list of regulated genes, we analyzed samples by gene set enrichment analysis to expand our results. A pool of spinal cord tissue from spina bifida fetuses whose mothers were exposed to RA was compared to a pool of spinal cord tissue from fetuses whose mothers were exposed to olive oil vehicle. Three replicates each.
2011-05-10 | E-GEOD-28834 | biostudies-arrayexpress
Project description:LC-MSMS (Label free) was performed to find differential proteins in maternal rat serum exosome between 3 normal pregnant rats and 3 pregnant rats carrying fetuses with spina bifida aperta induced by all-trans retinoic acid (Sigma; 4% [wt/vol] in olive oil; 140 mg/kg body weight by gavage) at pregnant day E18 (vaginal smear found sperm after mating as E0).
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