Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mapping the glial transcriptome in Huntington’s disease using snRNAseq: Selective disruption of glial signatures across brain regions

ABSTRACT: Mapping the glial transcriptome in Huntington’s disease using snRNAseq: Selective disruption of glial signatures across brain regions

PROVIDER: PRJNA1181917 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR31225800.fastq.gz	Fastqsanger.gz
	SRR31225801.fastq.gz	Fastqsanger.gz
	SRR31225802.fastq.gz	Fastqsanger.gz
	SRR31225803.fastq.gz	Fastqsanger.gz
	SRR31225804.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 88

Similar Datasets

Mapping the glial transcriptome in Huntington’s disease using snRNAseq: Selective disruption of glial signatures across brain regions

Project description:Huntington’s disease (HD) is an autosomal dominant neurodegenerative disease with a fatal outcome. There is accumulating evidence of a prominent role of glia in the pathology of HD, and we investigated this by conducting single nuclear RNA sequencing (snRNAseq) of human post mortem brain in four differentially affected regions; caudate nucleus, frontal cortex, hippocampus and cerebellum. Across 127,205 nuclei from donors with HD and age/sex matched controls, wefound heterogeneity of glia which is altered in HD. We describe prominent changes in the abundance of certain subtypes of astrocytes, microglia, oligodendrocyte precursor cells and oligodendrocytes between HD and control samples, and these differences are widespread across brain regions. Furthermore, we highlight possible mechanisms that characterise the glial contribution to HD pathology including depletion of myelinating oligodendrocytes, an oligodendrocyte-specific upregulation of the calmodulin-dependent 3’,5’-cyclic nucleotide phosphodiesterase 1A (PDE1A) and an upregulation of molecular chaperones as a cross-glial signature and a potential adaptive response to the accumulation of mutant huntingtin (mHTT). Our results support the hypothesis that glia have an important role in the pathology of HD, and show that all types of glia are affected in the disease.

2024-11-09 | GSE281069 | GEO

Mapping the glial transcriptome in Huntington's disease using snRNAseq: selective disruption of glial signatures across brain regions.

Project description:Huntington's disease (HD) is an autosomal dominant neurodegenerative disease with a fatal outcome. There is accumulating evidence of a prominent role of glia in the pathology of HD, and we investigated this by conducting single nuclear RNA sequencing (snRNAseq) of human post mortem brain in four differentially affected regions; caudate nucleus, frontal cortex, hippocampus and cerebellum. Across 127,205 nuclei from donors with HD and age/sex matched controls, we found heterogeneity of glia which is altered in HD. We describe prominent changes in the abundance of certain subtypes of astrocytes, microglia, oligodendrocyte precursor cells and oligodendrocytes between HD and control samples, and these differences are widespread across brain regions. Furthermore, we highlight possible mechanisms that characterise the glial contribution to HD pathology including depletion of myelinating oligodendrocytes, an oligodendrocyte-specific upregulation of the calmodulin-dependent 3',5'-cyclic nucleotide phosphodiesterase 1 A (PDE1A) and an upregulation of molecular chaperones as a cross-glial signature and a potential adaptive response to the accumulation of mutant huntingtin (mHTT). Our results support the hypothesis that glia have an important role in the pathology of HD, and show that all types of glia are affected in the disease.

| S-EPMC11492505 | biostudies-literature

Alteration of Autophagy and Glial Activity in Nilotinib-Treated Huntington’s Disease Patients

Project description:Alteration of Autophagy and Glial Activity in Nilotinib-Treated Huntington’s Disease Patients

| PRJNA1183370 | ENA

The spatial landscape of glial pathology and T-cell response in Parkinson’s disease substantia nigra [snRNAseq]

Project description:The spatial landscape of glial pathology and T-cell response in Parkinson’s disease substantia nigra [snRNAseq]

| PRJNA1065855 | ENA

Right atrial snRNAseq analysis

Project description:Right atrial snRNAseq analysis

| PRJNA1236287 | ENA

hESC-based human glial chimeric mice reveal glial differentiation defects in Huntington disease

Project description:Huntington’s disease (HD) is characterized by hypomyelination as well as by neuronal loss. To assess the basis for white matter involution in HD, we generated bipotential glial progenitor cells (GPCs) from human embryonic stem cells (hESCs), derived from either huntingtin (mHTT)-mutant embryos or normal controls, and performed RNA sequence analysis to assess mHTT-dependent changes in gene expression. In hGPCs derived from 3 distinct mHTT-expressing hESC lines, a set of transcription factors associated with glial differentiation and myelin synthesis was sharply down-regulated, relative to normal hESC GPCs. In particular, NKX2.2, OLIG2, SOX10 and MYRF were all suppressed, with the consequent diminution of myelinogenesis-associated transcription. Accordingly, when mHTT-expressing hGPCs were transplanted into hypomyelinated shiverer mice, the resultant mHTT glial chimeras were hypomyelinated. The mHTT hGPCs also manifested impaired astrocytic differentiation, and developed abnormal fiber domain architecture. These data suggest that white matter involution in HD is a product of a cell-autonomous mHTT-dependent suppression of both astrocytic and oligodendrocytic differentiation by affected GPCs.

2018-11-10 | GSE105041 | GEO

Selective Disruption of Core Regulatory Transcription

Project description:Selective Disruption of Core Regulatory Transcription

| PRJNA494422 | ENA

snRNAseq of human limbus tissue

Project description:snRNAseq of human limbus tissue

| PRJNA935339 | ENA

snRNAseq in human fetal neocortex

Project description:snRNAseq in human fetal neocortex

| PRJNA885818 | ENA

Glia detect and transiently protect against dendrite substructure disruption

Project description:Glia assess axon structure to modulate myelination and axon repair. Whether glia similarly detect dendrites and their substructures is not well understood. Here, we show that glia monitor the integrity of dendrite substructures and transiently protect their perturbation. We demonstrate that disruption of C. elegans sensory neuron dendrite cilia elicits acute glial responses, including increased accumulation of glia-derived extracellular matrix around cilia, changes in gene expression, and alteration of secreted protein repertoire. DGS-1, a 7-transmembrane domain neuronal protein, and FIG-1, a multifunctional thrombospondin-domain glial protein, are required for glial detection of cilia integrity, physically interact, and exhibit mutually-dependent localization to and around cilia, respectively. Glial responses to dendrite cilia disruption transiently protect against damage. Thus, our studies uncover a homeostatic, protective, dendrite glia signaling interaction regulating dendrite substructure integrity.

2024-12-06 | GSE282640 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data