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Activation of M3 muscarinic ameliorates experimental autoimmune encephalomyelitis by restoring microglial quiescence

GSE298934 Mus musculus (mouse) RNA-seq (gene expression) 9 samples Submitted 2026/06/01 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 9 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
9 samples: 3 × BV2, Control, biol vs 3 × BV2, LPS, biol vs 3 × BV2, LPS+Pilo, biolGroups are read from the sample names, not from the paper. Check the list below.
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)
The cholinergic system serves as a crucial signaling mediator in neuroimmune regulation. Our previous study has shown that muscarinic acetylcholine receptors (mAChRs) contributed to microglial inflammatory response. However, its role in autoimmune neurodegeneration, such as multiple sclerosis (MS) remains unclear. In this study, we investigated the role of microglial mAChRs in MS pathology.
Read the full summary ↓
For downstream analysis, we employed high-throughput transcriptomic sequencing in lipopolysaccharide (LPS)-stimulated BV2 microglia cells treated with pilocarpine (Pilo), a agonist of mAChRs. LPS+Pilo-treated cells displayed a transcriptional profile with similarity to that of normal cells. Alterations in cell chemotaxis and immune responses, with the activation of multiple GPCR downstream signaling pathways and TNF signaling pathways are also seen in LPS+Pilo-treated cells compared with LPS-stimulated cells, with significantly different expression of Msr1, Cybb, Ccl12, and Nr4a1. The results revealed that activation of mAChRs in microglia significantly upregulates Nr4a1 expression, which subsequently suppresses NF-κB-mediated inflammatory signaling.
This dataset
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.

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 GSE298934_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA1271957 and SRA study SRP589808. Searching any of these in the dataset finder brings you back here.

Study design
3 × BV2, Control, biol vs 3 × BV2, LPS, biol vs 3 × BV2, LPS+Pilo, biol

Supports a between-group comparison across 9 samples.

How we read this: 3 replicated groups read from 9 sample titles; they account for 9 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
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