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Endothelial UCP2 regulates the neurogenic-to-astrogenic fate switch during brain development

ABSTRACT: Endothelial UCP2 regulates the neurogenic-to-astrogenic fate switch during brain development

PROVIDER: PRJNA770299 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16295317_1.fastq.gz	Fastqsanger.gz
	SRR16295317_2.fastq.gz	Fastqsanger.gz
	SRR16295318_1.fastq.gz	Fastqsanger.gz
	SRR16295318_2.fastq.gz	Fastqsanger.gz
	SRR16295319_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Endothelial UCP2 regulates the neurogenic-to-astrogenic fate switch during brain development

Project description:Purpose: To gain futher insight into how endothelial UCP2 regulates the neurogenic-to-astrogenic fate switch ,RNA-seq was used to analyze the genome-wide changes resulting from isolated endothelial cells of E14.5 and E17.5 UCP2 endothelial conditional knock out mice and littermate wild-type. Methods: mRNA from E15 and E18 isolated endothelial cells of wild-type(WT) and UCP2f/f;Tie2-cre mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, mRNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics Results: Approximately one thousand transcripts showed differential expression between the wild-type(WT) and UCP2ECKO mice brain cortex, with a fold change ≥2 and p value <0.05.Geneontology analysis of the up-regulated genes showed obvious enrichment of biological processes related to development process and regulation of cell communication.The down-regulated genes exhibited enrichment of biological processes related to cell fate commitment. These results reflected endothelial UCP2 plays roles in cortex development. Conclusions: Endothelial UCP2 RNA-seq would provide a overall understanding how endothelial UCP2 regulates the neurogenic-to-astrogenic fate switch during brain development

2021-10-13 | GSE185656 | GEO

Endothelial Cells Mediated by UCP2 Control the Neurogenic-to-Astrogenic Neural Stem Cells Fate Switch During Brain Development.

Project description:During mammalian cortical development, neural stem/progenitor cells (NSCs) gradually alter their characteristics, and the timing of generation of neurons and glial cells is strictly regulated by internal and external factors. However, whether the blood vessels located near NSCs affect the neurogenic-to-gliogenic transition remain unknown. Here, it is demonstrated that endothelial uncoupling protein 2 (UCP2) deletion reduces blood vessel diameter and affects the transition timing of neurogenesis and gliogenesis. Deletion of endothelial UCP2 results in a persistent increase in astrocyte production at the postnatal stage. Mechanistically, the endothelial UCP2/ROS/ERK1/2 pathway increases chymase-1 expression to enhance angiotensin II (AngII) secretion outside the brain endothelium. The endotheliocyte-driven AngII-gp130-JAK-STAT pathway also regulates gliogenesis initiation. Moreover, endothelial UCP2 knockdown decreases human neural precursor cell (hNPC) differentiation into neurons and accelerates hNPC differentiation into astrocytes. Altogether, this work provides mechanistic insights into how endothelial UCP2 regulates the neurogenic-to-gliogenic fate switch in the developing neocortex.

| S-EPMC9218656 | biostudies-literature

Hdac3 Interaction with p300 Histone Acetyltransferase Regulates the Oligodendrocyte and Astrocyte Lineage Fate Switch (ChIP-Seq)

Project description:Establishment and maintenance of CNS glial cell identity ensures proper brain development and function, yet the epigenetic mechanisms underlying glial fate control remain poorly understood. Here we show that the histone deacetylase Hdac3 controls oligodendrocyte-specification gene Olig2 expression, and functions as a molecular switch for oligodendrocyte and astrocyte lineage determination. Our data suggest that Hdac3 cooperates with p300 to prime and maintain oligodendrogenic programs while inhibiting Stat3-mediated astrogliogenesis, and thereby regulate phenotypic commitment at the point of oligodendrocyte-astrocytic fate decision. Examination of Hdac3 and p300 genomewide occupancy in differentiating oligodendrocytes

2016-02-21 | E-GEOD-76411 | biostudies-arrayexpress

Intron detention tightly regulates the stemness/differentiation switch in the adult neurogenic niche

Project description:Intron detention tightly regulates the stemness/differentiation switch in the adult neurogenic niche

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Hdac3 Interaction with p300 Histone Acetyltransferase Regulates the Oligodendrocyte and Astrocyte Lineage Fate Switch (RNA-Seq)

Project description:Establishment and maintenance of CNS glial cell identity ensures proper brain development and function, yet the epigenetic mechanisms underlying glial fate control remain poorly understood. Here we show that the histone deacetylase Hdac3 controls oligodendrocyte-specification gene Olig2 expression, and functions as a molecular switch for oligodendrocyte and astrocyte lineage determination. Our data suggest that Hdac3 cooperates with p300 to prime and maintain oligodendrogenic programs while inhibiting Stat3-mediated astrogliogenesis, and thereby regulate phenotypic commitment at the point of oligodendrocyte-astrocytic fate decision. Gene expression profiling of optic nerve from P12 control and Hdac3 cKO mice

2016-02-21 | E-GEOD-76410 | biostudies-arrayexpress

Transcriptome Sequencing During Mouse Brain Development Identifies Long Non-Coding RNAs Functionally Involved in Neurogenic Commitment

Project description:Transcriptome analysis of somatic stem cells and their progeny is fundamental to identify new factors controlling proliferation versus differentiation during tissue formation. Here we generated a combinatorial, fluorescent reporter mouse line to isolate proliferating neural stem cells, differentiating progenitors and newborn neurons that coexist as intermingled cell populations during brain development. Transcriptome sequencing revealed numerous novel long non-coding (lnc)RNAs and uncharacterized protein-coding transcripts identifying the signature of neurogenic commitment. Importantly, most lncRNAs overlapped neurogenic genes and shared with them a nearly identical expression pattern suggesting that lncRNAs control corticogenesis by tuning the expression of nearby cell fate determinants. We assessed the power of our approach by manipulating lncRNAs and protein-coding transcripts with no function in corticogenesis reported to date. This led to several evident phenotypes in neurogenic commitment and neuronal survival indicating that our study provides a remarkably high number of uncharacterized transcripts with hitherto unsuspected roles in brain development. Finally, we focussed on one lncRNA, Miat, whose manipulation was found to trigger pleiotropic effects on brain development and aberrant splicing of Wnt7b. Hence, our study suggests that lncRNA-mediated alternative splicing of cell fate determinants controls stem cell commitment during neurogenesis. M-bM-^@M-^\LncRNAs control neurogenesisM-bM-^@M-^] Aprea, Prenninger, Dori, Monasor, Wessendof, Zocher, Massalini, Ghosh, Alexopoulou, Lesche, Dahl, Groszer, Hiller, Calegari, The EMBO Journal (In Press) mRNA profiles of Proliferating Progenitors, Differentiating Progenitors and Neurons from lateral cortex of E14.5 mouse embryos. Each cell type in three biological replicates.

2013-11-18 | E-GEOD-51606 | biostudies-arrayexpress

Transcriptomic trajectory of the tendon and fibrocartilage fate switch

Project description:Transcriptomic trajectory of the tendon and fibrocartilage fate switch

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Hdac3 Interaction with p300 Histone Acetyltransferase Regulates the Oligodendrocyte and Astrocyte Lineage Fate Switch (ChIP-Seq)

2016-02-21 | GSE76411 | GEO

Hdac3 Interaction with p300 Histone Acetyltransferase Regulates the Oligodendrocyte and Astrocyte Lineage Fate Switch (RNA-Seq)

2016-02-21 | GSE76410 | GEO

Activation of quiescent neurogenic niches of aging brain

Project description:Proposals for induced glia-to-neuron conversion have raised the potential for generating new neurons to replace those lost due to injury, aging or neurodegenerative diseases. Here, single-cell spatial transcriptomics [Multiplexed Error Robust Fluorescence In Situ Hybridization (MERFISH)] is used to construct a spatial cell atlas of the subventricular and dentate gyrus neurogenic niches of young and aged adult murine brain. RNAs that encode the RNA binding protein Polypyrimidine Tract-Binding Protein (PTBP1) in the aged murine brain are determined to be highest in glia that line previously active neurogenic niches. A glial cell population with ependymal character within an initially quiescent subventricular neurogenic niche in the aged murine brain is identified that upon transient suppression of PTBP1 reenters the cell cycle, replicates DNA, and converts into neurons through a canonical adult neurogenesis pathway. Glia-derived neurons migrate from this niche, with some neurons transiting to the striatum and acquiring a transcriptome characteristic of GABAergic inhibitory neurons. Similar PTBP1 expressing quiescent glia are identified in the corresponding neurogenic niche of aged human brain. Thus, transient reduction of PTBP1 holds potential for inducing the generation of new neurons in quiescent neurogenic niches of the aged nervous system, thereby offering promising therapeutic applications.

2024-01-09 | GSE252835 | GEO

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