Signal requirement for cortical potential of transplantable human neuroepithelial stem cells [array]
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PROVIDER: PRJNA768415 | ENA |
REPOSITORIES: ENA
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Project description:Signal requirement for cortical potential of transplantable human neuroepithelial stem cells
| PRJNA763125 | ENA
Project description:The cerebral cortex develops from dorsal forebrain neuroepithelial progenitor cells. Initial expansion of the progenitor cell pool is followed by the generation of neurons of all the cortical layers and later, astrocytes and oligodendrocytes. However, the regulatory pathways that control the expansion and maintenance of the neuroepithelial progenitor cell pool are currently unknown. Here we define six basic pathway components that regulate proliferation of cortically specified human neuroepithelial stem cells (cNESCs) in vitro without the loss of developmental potential. We show that activation of FGF and inhibition of BMP and ACTIVIN A signalling are required for long-term cNESC proliferation. We also demonstrate that cNESCs preserve dorsal telencephalon-specific potential when GSK3, AKT and nuclear CATENIN-b1 activity are low. Remarkably, regulation of these six pathway components supports the clonal expansion of cNESCs. Moreover, cNESCs differentiate to lower and upper layer cortical neurons both in vitro and in vivo. Identifying the mechanisms that drive the self-renewal and fate of cNESCs decision of neuroepithelial stem cells is key to developing new stem cell-based therapeutic approaches to treat neurological conditions.
2022-02-04 | GSE184081 | GEO
Project description:The cerebral cortex develops from dorsal forebrain neuroepithelial progenitor cells. Initial expansion of the progenitor cell pool is followed by the generation of neurons of all the cortical layers and later, astrocytes and oligodendrocytes. However, the regulatory pathways that control the expansion and maintenance of the neuroepithelial progenitor cell pool are currently unknown. Here we define six basic pathway components that regulate proliferation of cortically specified human neuroepithelial stem cells (cNESCs) in vitro without the loss of developmental potential. We show that activation of FGF and inhibition of BMP and ACTIVIN A signalling are required for long-term cNESC proliferation. We also demonstrate that cNESCs preserve dorsal telencephalon-specific potential when GSK3, AKT and nuclear CATENIN-b1 activity are low. Remarkably, regulation of these six pathway components supports the clonal expansion of cNESCs. Moreover, cNESCs differentiate to lower and upper layer cortical neurons both in vitro and in vivo. Identifying the mechanisms that drive the self-renewal and fate of cNESCs decision of neuroepithelial stem cells is key to developing new stem cell-based therapeutic approaches to treat neurological conditions. In this study, we performed Oxford Nanopore technologies long-read RNA-sequencing (lrRNA-seq) of human cNESCs and of the human embryonic stem cells used to generate them. Two hESC cell lines were differentiated to cNESCs, which were then maintained in either six factors (6F : BMPRi, TGFBRi, GSK3i, FGF, TANKYRASEi, AKTi) or 4 factors (6F-2F : BMPRi, TGFBRi, GSK3i, FGF). All samples (hESCs, cNESCs in 6 factors, cNESCs in 4 factors) are submitted to lrRNA-seq as duplicates.
2022-02-04 | GSE185258 | GEO
Project description:In this study, we found that ablation of genes encoding ciliary transport proteins such as intraflagellar transport homolog 88 (Ift88) and kinesin family member 3a (Kif3a) in cortical radial progenitors led to periventricular heterotopia during late mouse embryogenesis. Conditional mutation of primary cilia unexpectedly caused breakdown of both the neuroepithelial lining and the blood-choroid plexus barrier. Choroidal leakage was partially caused by enlargement of the choroid plexus in the cilia mutants. We found that the choroid plexus expressed platelet-derived growth factor A (Pdgf-A) and that Pdgf-A expression was ectopically increased in cilia-mutant embryos. Cortices obtained from embryos in utero electroporated with Pdgfa mimicked periventricular heterotopic nodules of the cilia mutant.
2023-01-10 | PXD038557 | Pride
Project description:Generation of cortical neurons through large-scale expanding neuroepithelial stem cell from human pluripotent stem cells
| PRJNA714639 | ENA
Project description:Genome-wide DNA methylation profiling of 8 low-grade neuroepithelial tumors (LGNET) with FGFR2 fusions with various histologic diagnoses including ganglioglioma, multinodular and vacuolating neuronal tumor (MVNT), low-grade glioneuronal tumor NOS, and polymorphous low-grade neuroepithelial tumor of the young (PLNTY). The Illumina Infinium EPIC 850k Human DNA Methylation Beadchip was used to obtain DNA methylation profiles across approximately 850,000 CpG sites of genomic DNA extracted from formalin-fixed, paraffin-embedded tumor tissue of 8 low-grade neuroepithelial tumors with FGFR2 fusions.
2021-07-27 | GSE172081 | GEO
Project description:WDR12 is a ribosome biogenesis factor known to be expressed in Optic tectum Neuroepithelial cells, we define the transcriptome profile of the optic tectum neuroepithelial cells, by cell-sorting followed by RNA-seq (Illumina technology).
2019-04-20 | GSE80497 | GEO
Project description:Genome-wide DNA methylation profiling of 30 low-grade neuroepithelial tumors with FGFR1 alterations including rosette-forming glioneuronal tumor, pilocytic astrocytoma, dysembryoplastic neuroepithelial tumor, and extraventricular neurocytoma. The Illumina Infinium EPIC 850k Human DNA Methylation Beadchip was used to obtain DNA methylation profiles across approximately 850,000 CpG sites of genomic DNA extracted from formalin-fixed, paraffin-embedded tumor tissue of 30 low-grade neuroepithelial tumors with FGFR1 alterations including kinase domain tandem duplication, in-frame fusion with TACC1, and hotspot missense mutation within the intracellular tyrosine kinase domain.
2020-08-19 | GSE152653 | GEO
Project description:Comparing gene expressing profile of human embryonic stem cells and neuroepithelial cells differentiated from human embryonic stem cells.
2009-11-08 | E-MEXP-2426 | biostudies-arrayexpress
Project description:The transcriptional coactivator Yap promotes proliferation and inhibits apoptosis, suggesting that Yap functions as an oncogene. Most oncogenes, however, require a combination of at least two signals to promote proliferation. Here we present evidence that Yap activation is insufficient to promote growth in the otherwise normal tissue. Using a mosaic mouse model, we demonstrate that Yap overexpression in a fraction of hepatocytes does not lead to their clonal expansion, as proliferation is counterbalanced by increased apoptosis. To shift the activity of Yap towards growth, a second signal provided by tissue damage or inflammation is required. In response to liver injury, Yap drives clonal expansion, suppresses hepatocyte differentiation and promotes a progenitor phenotype. These results suggest that Yap activation is insufficient to promote growth in the absence of a second signal thus coordinating tissue homeostasis and repair. Totally sixteen samples
2015-02-07 | E-GEOD-65207 | biostudies-arrayexpress