GEO series

MicroRNA-150 controls experimental autoimmune encephalomyelitis by regulating CD4 T cell differentiation and function [RNA-seq I]

GSE167868 Mus musculus (mouse) RNA-seq (gene expression) 25 samples Submitted 2025/01/01 Platform GPL24247

At a glance

RNA-seq (gene expression) · mouse · 25 samples

What it is: RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism: Mus musculus (mouse)
Samples: 25 samples
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.

Summary (written by the submitters)

MicroRNAs are small non-coding RNA molecules that have an important role in the fine tuning of all biological processes and are often found to be dysregulated in diseases, such as multiple sclerosis (MS). MS is an immune-mediated disease of the central nervous system characterized by demyelination, axonal loss and neurodegeneration. We have previously shown microRNA-150 (miR-150) levels to be elevated in cell-free cerebrospinal fluid (CSF) of MS patients compared to controls.

Read the full summary ↓

The aim of this study is to further understand the physiopathological function of miR-150 using experimental autoimmune encephalomyelitis (EAE), a mouse model for MS. To establish its role in-vivo, we generated miR-150 knock-out (KO) and knock-in (KI) mice using CRISPR/Cas9. After induction of EAE, miR-150 KO mice showed ameliorated disease compared to WT littermate controls while miR-150 KI mice presented with exacerbated disease. An ameliorated disease in miR-150 KO was accompanied by a decreased infiltration of CD4 T cells compared to WT and KI. At priming stage of EAE we found that miR-150 KO had an increase in regulatory CD4 T cells (TREGS). Furthermore, after reconstitution of T cell deficient animals, CD4 T cells from miR-150 KO mice could protect against EAE and also showed an increased FOXP3 expression. A role of miR-150 in regulating TREG cells was further substantiated by transcriptome profiling, where miR-150 KO CD4 T cells suggested an enhancement of TREG phenotype as well as a diminished translation in miR-150 KO CD4 T cells. Moreover the results implicated miR-150 with mechanisms such as translation, autophagy and metabolism as well T cell proliferation and differentiation. In conclusion, miR-150 deficiency favored a more anti-inflammatory environment while miR-150 expression promoted pathogenic CD4 T cells subsets, potentially associated with metabolic mechanisms.

This dataset

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Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE167868_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA705360 and SRA study SRP308487. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

The sample list for this study is not cached yet. Press Load samples and it will be fetched from NCBI.

+ 25 more — browse all 25 samples with per-sample file links →

Datasets on a similar topic

GSE227844 MicroRNA-150 controls experimental autoimmune encephalomyelitis by regulating CD4 T cell differentiation and function [RNA-seq II] 44 samples shares cd4, encephalomyelitis, microrna-150, experimental, autoimmune, regulating, controls, rna-seq
GSE227937 MicroRNA-150 controls experimental autoimmune encephalomyelitis by regulating CD4 T cell differentiation and function 69 samples shares cd4, encephalomyelitis, microrna-150, experimental, autoimmune, regulating, controls
GSE287323 Transcriptomic profiling of oligodendrocytes, astrocytes, and microglia in an experimental autoimmune encephalomyelitis (EAE) model of demyelination 19 samples shares encephalomyelitis, experimental, autoimmune
GSE326335 Bulk RNA Sequencing of Chimera-Derived Monocyte-Derived Macrophages Targeted for Mitochondrial ROS During Peak Experimental Autoimmune Encephalomyelitis 14 samples shares encephalomyelitis, experimental, autoimmune
GSE324711 An adaptive cellular source of IL-17A and IL-17F is critical for the induction of experimental autoimmune encephalomyelitis I 12 samples shares encephalomyelitis, experimental, autoimmune
GSE262540 Myelin oligodendrocyte glycoprotein reactive Th17 cells drive Janus Kinase 1 dependent transcriptional reprogramming in astrocytes and alter cell surface cytokine receptor profiles during experimental autoimmune encephalomyelitis. 12 samples shares encephalomyelitis, experimental, autoimmune
GSE287324 Transcriptomic analysis of spinal cord in day 35 experimental autoimmune encephalomyelitis (EAE) model 10 samples shares encephalomyelitis, experimental, autoimmune
GSE298934 Activation of M3 muscarinic ameliorates experimental autoimmune encephalomyelitis by restoring microglial quiescence 9 samples shares encephalomyelitis, experimental, autoimmune

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.