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Inhibition of p38 MAPK after repetitive mild TBI ameliorates immune signaling and behavioral deficit

GSE298240 Mus musculus (mouse) RNA-seq (gene expression) 58 samples Submitted 2026/03/18 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 58 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
58 samples: 8 conditions, mostly with about 8 replicates eachGroups 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
Inhibition of p38 MAPK after repetitive mTBI ameliorates immune signaling and functional deficitsActa neuropathologica communications · 2026
Summary (written by the submitters)
Background: Mild head injury associated with long-term functional impairments (i.e., depression, anxiety) is frequently observed among patients who experienced mild traumatic brain injury (mTBI). Moreover, repetitive injuries within a window of vulnerability can lead to exacerbated consequences compared to a single mTBI. However, current interventions for mTBI focus on alleviating symptoms, rather than targeting underlying mechanisms.
Read the full summary ↓
Following the initial mechanical impact, increasing evidence suggests that the brain undergoes an inflammatory cascade consisting of pro-inflammatory intracellular signaling pathways and production of cytokines, ultimately leading to chronic neuroinflammation and persistent neurological deficits, such as depression. Specifically, in the context of severe brain injury, the p38 MAPK signaling pathway has been identified as a key driver to the inflammatory response, associated with increased microglial activation, proinflammatory cytokines, and synaptic dysfunctions, but its role in the context of mild brain injury remains unclear. As such, this study aimed to investigate whether p38 MAPK drives the inflammatory responses and longer-term deficits following a weight-drop mouse model of repetitive mTBI (rmTBI). Methods: We injected C57/BL6 mice with SB239063, a small molecule p38 MAPK inhibitor, after each of the 5 once-daily weight-drop closed head injuries (CHIs) or sham. We evaluated functional outcomes within 4-weeks after the final CHI and quantified cytokine expressions, microglia reactivity, and transcriptional profiles at 4hr and 4-weeks post final injury. Results: We found that in females, acute inhibition of p38 MAPK attenuated acute inflammatory response comprised of increased cytokine/chemokine expression and microglial activation at 4-hours post injury and longer-term anti-depressive-like behavioral at 4-weeks post injury. However, such effects of p38 inhibition were less obvious in males. On the transcript level, we found that p38 inhibition not only normalized the effects of the brain injury but also upregulated protective genes and pathways associated with recovery and the maintenance of brain homeostasis. Together, these findings support the therapeutic potential of p38 MAPK inhibition following (r)mTBI, indicating the role of p38 MAPK in driving the acute and longer-term consequences post brain injury in a sex dependent manner.
Published in
Inhibition of p38 MAPK after repetitive mTBI ameliorates immune signaling and functional deficits
Li C, Griffin MN, Triplett SE et al. · Acta neuropathologica communications 2026 · PMID 41618372 · doi:10.1186/s40478-026-02226-w
This dataset
Open GSE298240 in finder → Find more mouse 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 GSE298240_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 PRJNA1268557 and SRA study SRP587986. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41618372) ↗
Study design
8 conditions, mostly with about 8 replicates each
F_Chronic_5xCHI+ vehicle ×12 F_Chronic_5xCHI+ SB ×11 F_Chronic_sham+ vehicle ×9 M_Chronic_5xCHI+ SB ×8 M_Chronic_5xCHI+ vehicle ×8 M_Chronic_sham+ vehicle ×5 F_Chronic_sham+ SB ×3 M_Chronic_sham+ SB ×2

Supports a between-group comparison across 58 samples.

How we read this: 8 replicated groups read from 58 sample titles; they account for 58 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

+ 18 more — browse all 58 samples with per-sample file links →

Datasets on a similar topic

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