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Addressing human astrogliosis in a human iPSC-derived 3D CNS model

GSE243254 Homo sapiens (human) RNA-seq (gene expression) 20 samples Submitted 2025/07/02 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 20 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
20 samples: 5 conditions, mostly with about 4 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.
Summary (written by the submitters)
Astrogliosis is an inflammatory process by which astrocytes undergo morphological, transcriptional, and functional changes that primarily contribute to tissue healing and restore CNS homeostasis as a response to neuroinflammation. However, excessive astrocyte activation causes neuronal death, immune cell activation and infiltration, and chronic neuroinflammation.
Read the full summary ↓
The advent of human induced pluripotent stem cell (hiPSC)-derived three-dimensional (3D) models has aided research of complex CNS processes by generating complex structures of neural cells able to decode the molecular mechanisms that trigger and sustain astrocyte activation and drive microenvironment remodeling in the human CNS. Despite depicting interactions between different brain cell types and their microenvironment, the lack of reproducibility, and immature/activated cell phenotypes typical of these models limit their utility to address neuroinflammation mechanisms. Here we establish a hiPSC-derived model of neuroinflammation to dissect cellular crosstalk along the neuroinflammatory axis. A methodology pioneered by our team was used, in which hiPSC-derived neural progenitors were cultured in perfusion stirred-tank bioreactors and differentiated into 3D neurospheroids composed of neurons, astrocytes, and oligodendrocytes. This model recapitulates specific features of the brain microenvironment, such as human brain-like ECM deposition and neuron-glia functional interactions. The neurospheroids were challenged with prototypical inflammatory factors reported to induce activation of astrocytes in mice models, namely TNF-α, IL-α, and C1q. By performing whole transcriptome analysis (RNAseq), we observed an upregulation of several inflammatory-related genes associated with TNF and NF-kB signaling (e.g., CXCL5, CCL2, TNAIP3, and NFKB2). Whole proteome analysis (SWATH-MS) also depicted the enrichment of proteins involved in cell response to stress and cytokine regulation, namely TXLNA, DCTN5, and NOLC1. Concomitantly, time course analysis of conditioned media from the stimulated neurospheroids exhibited increased secretion of inflammation-related cytokines (e.g., CCL2, CXCL10, IL-6, and IL-8). Astrocytes in challenged neurospheroids displayed an impaired capacity for clearance of extracellular glutamate and secretion of glutamine compared to the unstimulated control, indicating functional impairment and known molecular effects of TNF signaling. Together, these results further demonstrate astrocyte functionality within the neurospheroids, which undergo canonical astrogliosis events that are considered hallmarks of neuroinflammation. The human neurospheroid model described may contribute to better understand the mechanisms governing human astrogliosis and be used as a platform to study glial-neuron mature interactions during acute stimulation and inflammation.
This dataset
Open GSE243254 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 GSE243254_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 PRJNA1017481 and SRA study SRP460655. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
5 conditions, mostly with about 4 replicates each
hiPSC-neurospheroids, day-0, control, ×4 hiPSC-neurospheroids, day-1, control, ×4 hiPSC-neurospheroids, day-3, control, ×4 hiPSC-neurospheroids, day-1, treated, ×4 hiPSC-neurospheroids, day-3, treated, ×4

Supports a case/control comparison: 8 samples read as cases, 12 as controls.

How we read this: 5 replicated groups read from 20 sample titles; they account for 20 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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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.