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Gene expression changes in cerebellar meninges in Pdgfc and Pdgfra mutant mice at P0

ABSTRACT: Platelet-derived growth factor-C (PDGF-C) is one of three known ligands for the tyrosine kinase receptor PDGFRα. We generated mice that were double mutants for Pdgfc -/- and Pdgfra GFP/+, and have previously shown how cerebral meninges are affected resulting in developmental neuronal overmigration. Other severe phenotypes displayed in these mice include cerebellar malformation, spina bifida and lung emphysema. We focused our analysis on the central nervous system (CNS) and the cerebellum, where PDGF-C was identified as a critical factor during development.

ORGANISM(S): Mus musculus Mus

PROVIDER: GSE202835 | GEO | 2022/07/28

REPOSITORIES: GEO

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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.

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Gene expression changes in cerebellar meninges in Pdgfc and Pdgfra mutant mice at P0

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