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Chronic exposure to glucocorticoids amplifies inhibitory neuron cell fate during human neurodevelopment in organoids [scATAC-seq]

ABSTRACT: Chronic exposure to glucocorticoids amplifies inhibitory neuron cell fate during human neurodevelopment in organoids [scATAC-seq]

PROVIDER: PRJNA1061108 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27422100_1.fastq.gz	Fastqsanger.gz
	SRR27422100_2.fastq.gz	Fastqsanger.gz
	SRR27422101_1.fastq.gz	Fastqsanger.gz
	SRR27422101_2.fastq.gz	Fastqsanger.gz
	SRR27422102_1.fastq.gz	Fastqsanger.gz

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Chronic exposure to glucocorticoids amplifies inhibitory neuron cell fate during human neurodevelopment in organoids.

Project description:Chronic exposure to glucocorticoids amplifies inhibitory neuron cell fate during human neurodevelopment in organoids.

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Chronic exposure to glucocorticoids amplifies inhibitory neuron cell fate during human neurodevelopment in organoids [scRNA-seq]

Project description:Chronic exposure to glucocorticoids amplifies inhibitory neuron cell fate during human neurodevelopment in organoids [scRNA-seq]

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Chronic exposure to glucocorticoids amplifies inhibitory neuron cell fate during human neurodevelopment in organoids [scATAC-seq]

Project description:Disruptions in the tightly regulated process of human brain development have been linked to increased risk for brain and mental illnesses. While the genetic contribution to these diseases is well established, important environmental factors have been less studied at molecular and cellular levels. In this study, we used single-cell and cell-type-specific techniques to investigate the effect of glucocorticoid (GC) exposure, a mediator of antenatal environmental risk, on gene regulation and lineage specification in unguided human neural organoids. We characterized the transcriptional response to chronic GC exposure during neural differentiation and studied the underlying gene regulatory networks by integrating single-cell transcriptomics- with chromatin accessibility data. We found lasting cell type-specific changes that included autism risk genes and several transcription factors associated with neurodevelopment. Chronic GCs influenced lineage specification primarily by priming the inhibitory neuron lineage through key transcription factors like PBX3. We provide evidence for convergence of genetic and environmental risk factors through a common mechanism of altering lineage specification.

2024-01-22 | GSE252523 | GEO

Chronic exposure to glucocorticoids amplifies inhibitory neuron cell fate during human neurodevelopment in organoids [scRNA-seq]

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Chronic exposure to glucocorticoids amplifies inhibitory neuron cell fate during human neurodevelopment in organoids.

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2024-01-22 | GSE252524 | GEO

5-hydroxymethylcytosine-mediated epigenetic dynamics during neurodevelopment and aging

Project description:This SuperSeries is composed of the following subset Series: GSE32050: 5-hydroxymethylcytosine-mediated epigenetic dynamics during neurodevelopment and aging [5hmC Capture and Seq] GSE32187: 5-hydroxymethylcytosine-mediated epigenetic dynamics during neurodevelopment and aging [mRNA profiling] Refer to individual Series

2011-10-29 | E-GEOD-32188 | biostudies-arrayexpress

scATAC-seq of mouse Plasmodium-specific CD4+ T cells

Project description:Plasmodium-specific CD4+ T cells from mice infected with Plasmodium chabaudi chabaudi AS parasites were recovered at Days 0, 4, 7, and 32 to undergo processing and to generate scATAC-seq dataset. At Day 7, CXCR5+ and CXCR6+ cells were recovered separately. At Day 32, mice were administered with either saline or artesunate (intermittent artesunate therapy - IAT). scATAC-seq dataset was analysed to investigate epigenomic landscapes of CD4+ T cells from effector to memory states.

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Yakimchuk2019 - Mathematical modeling of immune modulation by glucocorticoids

Project description:Mathematical modeling of immune modulation by glucocorticoids Konstantin Yakimchuk https://doi.org/10.1016/j.biosystems.2019.104066 Abstract The cellular and molecular mechanisms of immunomodulatory actions of glucocorticoids (GC) remain to be identified. Using our experimental findings, a mathematical model based on a system of ordinary differential equations for characterization of the regulation of anti-tumor immune activity by the both direct and indirect GC effects was generated to study the effects of GC treatment on effector CD8+ T cells, GC-generated tolerogenic dendritic cells (DC), regulatory T cells and the growth of lymphoma cells. In addition, we compared the data from in vivo and in silico experiments. The mathematical simulations indicated that treatment with GCs may suppress anti-tumor immune response in a dose-dependent manner. The model simulations were in line with earlier experimental observations of inhibitory effects of GCs on T and NK cells and DCs. The results of this study might be useful for predicting clinical outcomes in patients receiving GC therapy.

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