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Defective plasticity in dermatomyositis patients muscle stem cells is associated with sustained intrinsic inflammatory signaling and disruption of the histone H3.3 chromatin loading pathway [RNA-seq]

GSE298208 Homo sapiens (human) RNA-seq (gene expression) 24 samples Submitted 2025/06/08 Platform GPL34295
At a glance

RNA-seq (gene expression) · human · 24 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
Homo sapiens (human)
Samples
24 samples: 8 conditions, mostly in duplicateGroups 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.
Paper
Defective plasticity in dermatomyositis patients muscle stem cells is associated with sustained intrinsic inflammatory signaling and disruption of the histone H3.3 chromatin loading pathwayNAR molecular medicine · 2026
Summary (written by the submitters)
Skeletal muscle regeneration is driven by muscle stem cells (MuSC). They proliferate then differentiate to restore muscle function. This process, known as myogenesis, is driven both by intrinsic properties of MuSCs and by extrinsic inflammatory signals. While proinflammatory signals are necessary for healthy muscle regeneration, chronic inflammation participates in different pathologies affecting the skeletal muscle, including cancer-associated cachexia, Duchenne muscular dystrophy (DMD) or auto-immune disorders.
Read the full summary ↓
Dermatomyositis (DM) is characterized by infiltration of immune cells in the peri-fascicular area which is associated with chronic inflammation. Although anti-inflammatory treatments are commonly used to combat the disease, most patients never fully regain their muscle strength. MuSCs derived from dermatomyositis patients exhibit impaired myogenesis in vitro, indicating that these cells may have acquired intrinsic defects that contribute to the disease. We compared the transcriptomes of MuSCs from healthy individuals and DM patients, finding that the latter are unable to effectively execute the myogenic transcriptomic program during ex vivo differentiation. Additionally, they exhibit an intrinsically activated canonical TNF signaling. MuSC from DM patients also exhibit reduced expression of H3.3 and its chaperone genes, coupled with a decrease in H3.3 deposition across the entire genome. The global loss of H3.3 combined with elevated intrinsic TNF signaling is associated with a failure of DM-derived MuSCs to suppress inflammatory signals and achieve proper myogenesis, suggesting a mechanistic link between epigenetic dysregulation and defective muscle regeneration.
Published in
Defective plasticity in dermatomyositis patients muscle stem cells is associated with sustained intrinsic inflammatory signaling and disruption of the histone H3.3 chromatin loading pathway
Bouchereau W, Chenane L, Weiss-Gayet M et al. · NAR molecular medicine 2026 · PMID 42199921 · doi:10.1093/narmme/ugag022
This dataset
Open GSE298208 in finder → Find more human RNA-seq datasets →
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 GSE298208_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 PRJNA1268521 and SRA study SRP588052. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42199921) ↗
Study design
8 conditions, mostly in duplicate
HC-MuSC from patient CT6, Differentiation day ×2 HC-MuSC from patient CT7, Differentiation day ×2 HC-MuSC from patient SK230, Differentiation d… ×2 HC-MuSC from patient SK236, Differentiation d… ×2 DM-MuSC from patient sDM1, Differentiation day ×2 DM-MuSC from patient sDM3, Differentiation day ×2 DM-MuSC from patient sDM5, Differentiation day ×2 DM-MuSC from patient sDM6, Differentiation day ×2 +8 more

Supports a between-group comparison across 16 samples.

How we read this: 8 replicated groups read from 24 sample titles; they account for 16 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
Datasets on a similar topic

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