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Chronic administration of a HDAC inhibitor boosts microglial differentiation and treats neurological disease in a mouse model of intellectual disability.

GSE290539 Mus musculus (mouse) Single-cell RNA-seq 16 samples Submitted 2026/02/28 Platform GPL24247
At a glance

Single-cell RNA-seq · mouse · 16 samples

What it is
Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart. Read from the summary: GEO's own type field only says 'expression profiling by sequencing', so confirm it in the paper.
Organism
Mus musculus (mouse)
Samples
16 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)
Histone deacetylase inhibitors (HDACi) control chromatin states through histone acetylation and are of interest to treat neurological disorders. Defect in lysine-specific methyltransferase 2D (KMT2D) decreases the open chromatin mark H3K4me3 in brains of a mouse model of Kabuki Syndrome (KS), a rare intellectual disability disorder. We utilized single-cell RNA sequencing to explore the molecular landscape of microglia from the mouse hippocampus under different treatment conditions.
Read the full summary ↓
untreated, PEG [dimethyl sulfoxide, 5% (DMSO) and polyethylene glycol, 45% (PEG)], HPBCD [DMSO (5%), PEG (45%), Hydroxypropyl-β-cyclodextrin, 0.2 gm/ml (HPBCD)], and TCF [DMSO (5%), PEG (45%), HPBCD (0.2 gm/ml), Vorinostat (5 mg/ml, Vo)]. Administration of a brain-permeant triple combination formulation (TCF) of 2-hydroxypropyl-b-cyclodextrin (HPBCD), polyethylene glycol-400 (PEG) and the FDA-approved histone deacetylase inhibitor (HDACi), vorinostat, weekly over 3 months, increased microglial levels (but failed to stimulate hippocampal neurogenesis). The differential gene expression analysis in combination with ingenuity pathway analysis predicted the specific effect of TCF on microglial histone 3, whose acetylation restored H3K4me3 independent of Kmt2D.This study examines the impact of the histone deacetylase inhibitor (Vo as a brain permeant formulation) on microglia in a Kabuki syndrome model.
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 GSE290539_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: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1228588 and SRA study SRP566516. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 16 more — browse all 16 samples with per-sample file links →

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