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Expression data from proliferating and quiescent adult hippocampal neural stem and progenitor cells

ABSTRACT: Expression data from proliferating and quiescent adult hippocampal neural stem and progenitor cells

PROVIDER: PRJNA666143 | ENA |

REPOSITORIES: ENA

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Expression data from proliferating and quiescent adult hippocampal neural stem and progenitor cells

Project description:We have characterized the transcriptome of adult rat hippocampal neural stem and progenitor cell (NSPC) cultures. The NSPCs cultures can be reversibly arrested by the quiescence-promoting signal BMP4. We provide expression data from NSPCs grown as neurospheres for 4 days in vitro in the presence of FGF2 (proliferating NSPCs) or FGF2+BMP4 (quiescent NSPCs) showing that entry into quiescence involves major changes in the transcriptional profile of the cells.

2020-09-29 | GSE158658 | GEO

A fatty acid oxidation-dependent metabolic shift regulates adult neural stem cell quiescence

Project description:Adult hippocampal neurogenesis is important for certain forms of cognition and failing neurogenesis has been implicated in neuropsychiatric diseases. The neurogenic capacity of hippocampal neural stem/progenitor cells (NSPCs) depends on a balance between quiescent and proliferative states. However, how this balance is regulated remains poorly understood. Here we show that the rate of fatty acid oxidation (FAO) defines quiescence vs. proliferation in NSPCs. Quiescent NSPCs show high levels of carnitine palmitoyltransferase 1a (Cpt1a)-dependent FAO, which is downregulated in proliferating NSPCs. Pharmacological inhibition and conditional deletion of Cpt1a in vitro and in vivo leads to altered NSPC behavior, showing that Cpt1a-dependent FAO is required for stem cell maintenance and proper neurogenesis. Strikingly, experimental manipulation of malonyl-CoA, the metabolite that regulates levels of FAO, is sufficient to induce exit from quiescence and to enhance NSPC proliferation. Thus, the data presented here identify a shift in FAO metabolism that governs NSPC behavior and suggest an instructive role for fatty acid metabolism in regulating NSPC activity.

2019-11-15 | PXD005598 | Pride

Differential gene expression analysis between proliferating and quiescent human dermal fibroblasts

Project description:Purpose: Quiescence is a state or reversible cell cycle arrest. A previous study using microarrays (Coller et al., PMID: 16509772) revealed gene expression changes between quiescent and proliferating human dermal fibroblasts and defined a "quiescece program" of genes that change in abundance when fibroblasts were introduced into quiescence by one of three methods. The goal of this study is to perform high throughut RNA sequencing to determine global changes in gene expression between proliferating and quiescent human dermal fibroblasts. Methods: Three different biological replicates (corresponding to two fibroblast strains, 10-5 and 12-1) were collected in proliferating and contact--inhibited (quiescent) conditions. RNA extracted from these cells were used for library preparation. The libraries were sequenced on an Illumina HiSeq 2000 instrument. Results: Among the 19,673 genes monitored, 1,993 genes (10.1%) changed in expression two-fold or more, demonstrating widespread changes in gene expression with contact inhibition-induced quiescence. Fifty-two percent of these genes were upregulated in 7dCI compared with proliferating fibroblasts, and 48% were downregulated in 7dCI fibroblasts. Conclusions: There are widespread changes in gene expression as fibroblasts transition between proliferating and quiescent states.

2018-08-28 | GSE117444 | GEO

Inter-individual variation in genes governing human hippocampal progenitor differentiation is associated with hippocampal volume in adulthood

Project description:The aim of this study was to investigate the effects of the antidepressants, escitalopram (0 nM, 145 nM, 290 nM, 1160 nM) and nortriptyline (0 nM, 267 nM, 534 nM, 1068 nM), in human hippocampal progenitor cells (HPC0A07/03C), either when proliferating or differentiating. We also considered expression changes occuring when proliferating cells switch to a differentiating state to form young neurons and astrocytes.

2017-03-08 | GSE95791 | GEO

Genome-wide sequencing of REST binding (ChIP-seq) in adult hippocampal neural stem cells in vitro a.k.a. HCN cells in quiescent (iQNP) and proliferative (TAP) conditions

Project description:We report the high-throughput profiling of REST binding in mammalian adult hippocampal stem cells in culture (HCN cells). By obtaining 33 to 38 million single-end reads of sequence from chromatin immunoprecipitated DNA, we generated genome-wide REST binding state of HCN cells in induced quiescent (iQNP) and proliferating (TAP) conditions. Thereafter, we annotated the peaks to genomic regions and associated genes. We find that with +/-10kb of transcription start site of genes, REST efficiently binds neuronal genes and represses them in HCN cells in both iQNP and TAP conditions. Moreover, only in the iQNP REST also binds non-neuronal genes like DNA replication genes. This study reveals that in addition to its well known function as a neuronal repressor in non-neuronal tissue, REST can also play other diverse roles in non-neuronal tissues.

2016-11-09 | GSE70695 | GEO

Vascular Endothelial Growth Factor Receptor 3 (VEGFR3) controls hippocampal neural stem cell conversion into progenitor cells

Project description:Neural stem cells (NSCs) continuously produce new neurons within the adult mammalian hippocampus. However, this process declines with age and this decline correlates with defects in cognitive function and mood. Molecular mechanisms that activate quiescent NSCs to generate progenitor cells in vivo remain poorly understood. Here we show that adult hippocampal NSCs express VEGFR3, a key regulator of vascular and neural development, and are activated by the VEGFR3 ligand VEGF-C to enter the cell cycle and convert into progenitor cells. Conditional deletion of Vegfr3 in NSCs leads to a decline in hippocampal neurogenesis. Functionally, this is associated with increased anxiety behavior and compromised NSC activation in response to VEGF-C and physical activity. These findings establish VEGFR3 expression as a hallmark of adult mouse NSCs and demonstrate a specific requirement for VEGF-C/VEGFR signaling in NSC activation. Enhancing VEGFR3 signaling by VEGF-C may improve neurogenesis and mood during aging.

2014-03-06 | GSE55621 | GEO

Converged Epitranscriptomic Co-regulation of TGFβ Signaling Components Suppresses the Quiescence Transition of Early Postnatal Hippocampal Neural Stem Cells

Project description:Quiescence acquisition of proliferating neural stem cells (NSCs) is required to establish the adult NSC pool yet the underlying molecular mechanisms are not well-understood. Here we showed that conditional deletion of the m6A reader Ythdf2, which promotes mRNA decay, in proliferating NSCs in the early postnatal mouse hippocampus led to elevated quiescence acquisition with decreased neurogenesis. Multimodal profiling of m6A modification, YTHDF2 binding, and mRNA decay in hippocampal NSCs identified shared targets in multiple TGFβ signaling pathway components, including TGFβ ligands, maturation factors, receptors, transcription regulators, and signaling regulators. Functionally, Ythdf2 deletion led to TGFβ signaling activation in NSCs, suppression of which rescued elevated quiescence acquisition of proliferating hippocampal NSCs. Our study reveals the dynamic nature and critical roles of mRNA decay in establishing the quiescent adult hippocampal NSC pool and uncovers a novel mode of epitranscriptomic control via co-regulation of multiple components of the same signaling pathway.

2024-08-26 | GSE266096 | GEO

RNA-sequencing of mouse adult hippocampal progenitor cells in which Nfix was deleted.

Project description:RNA-sequencing of mouse adult hippocampal nestin+ progenitor cells & dcx+ progenitor cells from wild-type animals, and animals in which the gene Nfix was deleted.

2018-01-30 | GSE109817 | GEO

Mitochondrial pyruvate metabolism regulates the activation of quiescent adult neural stem cells

Project description:Cellular metabolism is important for adult neural stem/progenitor cell (NSPC) behavior. However, its role in the transition from quiescence to proliferation is not fully understood. We here show that the mitochondrial pyruvate carrier (MPC) plays a crucial and unexpected part in this process. MPC transports pyruvate into mitochondria, linking cytosolic glycolysis to mitochondrial tricarboxylic acid cycle and oxidative phosphorylation. Despite its metabolic key function, the role of MPC in NSPCs has not been addressed. We show that quiescent NSPCs have an active mitochondrial metabolism and express high levels of MPC. Pharmacological MPC inhibition increases aspartate and triggers NSPC activation. Furthermore, genetic Mpc1 ablation in vitro and in vivo also activates NSPCs, which differentiate into mature neurons, leading to overall increased hippocampal neurogenesis in adult and aged mice. These findings highlight the importance of metabolism for NSPC regulation and identify an important pathway through which mitochondrial pyruvate import controls NSPC quiescence and activation.

2023-01-26 | GSE220663 | GEO

Differential gene expression analysis between proliferating and quiescent human dermal fibroblasts

Project description:Differential gene expression analysis between proliferating and quiescent human dermal fibroblasts

| PRJNA482131 | ENA