Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A lysosomal regulatory circuit essential for the development and function of microglia

ABSTRACT: We performed Illumina NovaSeq on zebrafish larvae with or without Zymosan A injection

ORGANISM(S): Danio rerio

PROVIDER: GSE197348 | GEO | 2022/07/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

A lysosomal regulatory circuit essential for the development and function of microglia

Project description:We performed Illumina NovaSeq on macrophages isolated from zebrafish

2022-07-15 | GSE197349 | GEO

A lysosomal regulatory circuit essential for the development and function of microglia

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-15 | GSE197350 | GEO

A lysosomal regulatory circuit essential for the development and function of microglia

Project description:A lysosomal regulatory circuit essential for the development and function of microglia

| PRJNA809952 | ENA

A lysosomal regulatory circuit essential for the development and function of microglia

Project description:A lysosomal regulatory circuit essential for the development and function of microglia

| PRJNA809950 | ENA

A lysosomal regulatory circuit essential for the development and function of microglia

Project description:A lysosomal regulatory circuit essential for the development and function of microglia

| PRJNA809951 | ENA

Lipid-induced lysosomal damage after demyelination corrupts microglia protective function in lysosomal storage disorders.

Project description:Neuropathic lysosomal storage disorders (LSDs) present with activated pro-inflammatory microglia. However, anti-inflammatory treatment failed to improve disease pathology. We characterise the mechanisms underlying microglia activation in Niemann-Pick disease type A (NPA). We establish that an NPA patient and the acid sphingomyelinase knockout (ASMko) mouse model show amoeboid microglia in neurodegeneration-prone areas. In vivo microglia ablation worsens disease progression in ASMko mice. We demonstrate the coexistence of different microglia phenotypes in ASMko brains that produce cytokines or counteract neuronal death by clearing myelin debris. Overloading microglial lysosomes through myelin debris accumulation and sphingomyelin build-up induces lysosomal damage and cathepsin B extracellular release by lysosomal exocytosis. Inhibition of cathepsin B prevents neuronal death and behavioural anomalies in ASMko mice. Similar microglia phenotypes occur in a Niemann-Pick disease type C mouse model and patient. Our results show a protective function for microglia in LSDs and how this is corrupted by lipid lysosomal overload. Data indicate cathepsin B as a key molecule mediating neurodegeneration, opening research pathways for therapeutic targeting of LSDs and other demyelinating diseases.

| S-EPMC6331723 | biostudies-literature

Single-cell RNA sequencing of the cut and uncut caudal fin of zebrafish larvae

Project description:Purpose: The goal of this study was to establish the first detailed cell atlas of the regenerating caudal fin of zebrafish larvae. Intact and regenerating caudal fin were used for single-cell RNA-sequencing with the aim to provide the first integrated model of epimorphic regeneration in zebrafish larvae and demonstrate the diversity of the cells required for blastema formation. Methods: 150 of regenerating caudal fin (cut) and intact caudal fine (uncut) samples were dissociated and loaded into the 10x Genomics Chromium Platform, and sequenced using Illumina NovaSeq 6000. Conclusion: Our study constitutes a resource of the gene expression profile in intact and regenerating caudal fin of zebrafish larvae. We report the application of single-molecule-based sequencing technology for high-throughput profiling of both intact (uncut) and regenerating caudal fin samples (cut) at 24hpA. We confirmed the presence of macrophage subsets, previously described by our group to govern zebrafish fin regeneration, and identified a novel blastemal cell population.

2021-07-17 | GSE158851 | GEO

Lipid induced lysosomal damage after demyelination corrupts microglia protective function in Lysosomal Storage Disorders

Project description:Neuropathic Lysosomal Storage Disorders (LSDs) present with activated pro-inflammatory microglia. However, anti-inflammatory treatment failed to improve disease pathology. We characterise the mechanisms underlying microglia activation in Niemann Pick disease type A (NPA). We establish that an NPA patient and the Acid Sphingomyelinase knockout (ASMko) mouse model show amoeboid microglia in neurodegeneration-prone areas. In vivo microglia ablation worsens disease progression in ASMko mice. We demonstrate the coexistence of different microglia phenotypes in ASMko brains that produce cytokines or counteract neuronal death by clearing myelin debris. Overloading microglial lysosomes through myelin debris accumulation and sphingomyelin build up induces lysosomal damage and Cathepsin B extracellular release by lysosomal exocytosis. Inhibition of Cathepsin B prevents neuronal death and behavioural anomalies in ASMko mice. Similar microglia phenotypes occur in a Niemann Pick disease type C mouse model and patient. Our results show a protective function for microglia in LSDs and how this is corrupted by lipid lysosomal overload. Data indicate Cathepsin B as a key molecule mediating neurodegeneration, opening research pathways for therapeutic targeting LSDs and other demyelinating diseases.

| S-SCDT-EMBOJ-2018-99553 | biostudies-other

Transcriptomic Analysis of the Zebrafish Prion Mutants Supports Conserved Cross-Species Function of the Cellular Prion Protein

Project description:Wild-type zebrafish larvae and our prp1ua5003/ua5003;prp2ua5001/ua5001 mutant zebrafish larvae at 3 days post fertilisation were pooled into three biological replicates each of 50 larvae. Each replicate underwent paired end 100-125 and Illumina HiSeq2500 sequencing to a depth of 40 million reads, carried out by Otogenetics (Atlanta, GA). Samples were subsequently processed using the TopHat/Cufflinks bioinformatics pipeline. Alignments were mapped to the zebrafish reference genome, GRCz10. A small amount of wild-type reads were found to contaminate two of the pooled mutant samples and were not included in subsequent analysis. In total there were 1249 genes showing at least a 50% increase (745) in transcript abundance or 50% decrease (504) decrease in transcript abundance in wild-type zebrafish larvae compared to double mutant zebrafish larvae. Subsequent gene ontology analysis shows the biological process showing genes with the biggest decrease in transcript abundance was cell adhesion, and the process with the most genes showing an increase in transcript abundance was Oxidation/Reduction. Our study finds the processes affected by prion knockdown in zebrafish is remarkably similar to other studies in early mice embryos, suggesting a conserved function of the cellular prion protein in the early development of organisms.

2021-01-08 | GSE164423 | GEO

Cavin4/Murc is required for skeletal muscle development and function in zebrafish

Project description:To understand the underlying cause of the swimming defect in Cavin4/Murcb deficient larvae, we isolated mRNA from mutant and sibling zebrafish at 72 hpf and subjected it to microarray analysis. RNA and gDNA were extracted from individual larvae at 72 hpf using Trizol (Life Technologies). Following genotyping, the aqueous phases from at least 10 Trizol extractions were combined by genotype and purified over microspin columns (ZymoResearch). RNA expression from heterozygous and mutant larvae was analyzed by single-color microarray (8x60K Zebrafish Array XS, Oaklabs, Germany).

2015-07-14 | E-GEOD-70858 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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