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Cytokine Priming Enhances the Antifibrotic Effects of Mesenchymal Stromal Cells Conditioned Medium Via Fibrogenic Myofibroblasts Elimination and Extracellular Matrix Degradation.

GSE266052 Homo sapiens (human) RNA-seq (gene expression) 20 samples Submitted 2024/10/15 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 × Fibroblasts, Non-treated, vs 5 × Fibroblasts, TGF-β 72h, Non-treated 72h, vs 5 × Fibroblasts, TGF-β 72h, Resting hMSC(AT)-CM 72h, vs 5 × Fibroblasts, TGF-β 72h, Cytokine-primed hMSC(AT)-CM 72h,Groups 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
Cytokine priming enhances the antifibrotic effects of human adipose derived mesenchymal stromal cells conditioned mediumStem cell research & therapy · 2024
Summary (written by the submitters)
Background: Fibrosis is a pathological scarring process characterized by persistent myofibroblasts activation with excessive accumulation of extracellular matrix (ECM). Fibrotic disorders represent an increasing burden of disease-associated morbidity and mortality worldwide for which there are limited therapeutic options. Reversing fibrosis requires the elimination of myofibroblasts, remodeling of the ECM, and regeneration of functional tissue.
Read the full summary ↓
Multipotent mesenchymal stromal cells (MSC) have antifibrotic properties mediated by secreted factors present in their conditioned medium (MSC-CM). However, there are no standardized in vitro assays to predict the antifibrotic effects of human MSC, and, as a consequence, we lack evidence on the effect of cytokine priming on MSC’s antifibrotic effects. We hypothesize that the MSC-CM promotes fibrosis resolution in vitro and that this effect is enhanced following MSC cytokine priming. Methods: We tested the antifibrotic effects of resting and interferon gamma (IFN-γ) and tumor necrosis factor alpha (TNF-α) primed MSC-CM in three in vitro assays: prevention of fibroblast activation, myofibroblasts deactivation and ECM degradation. Furthermore, we performed transcriptomic analysis of myofibroblasts treated or not with resting- or primed-MSC-CM and proteomic characterization of resting- and primed-MSC-CM. Results: We report that MSC-CM treatment prevented TGF-β induced fibroblast activation and reduced fibrogenic myofibroblasts (i.e. transcriptomic upregulation of apoptosis, senescence, and inflammatory pathways). These effects were higher when primed rather than resting MSC-CM was used. Priming increased the ability of MSC-CM to remodel the extracellular matrix reducing its content of collagen I and fibronectin. Priming increased the following antifibrotic proteins in MSC-CM: DKK1, MMP-1, MMP-3, follistatin and cathepsin S. DKK1 inhibition reduced the anti-fibrotic effects of MSC-CM. Thus, cytokine priming increases antifibrotic factors in the MSC-CM which in turn amplify the anti-fibrotic effects of MSC-CM. Conclusions: In a pro-fibrotic in vitro environment MSC-CM promote fibrosis resolution, an effect enhanced following MSC cytokine priming. Specifically, MSC-CM reduces fibrogenic myofibroblasts through apoptosis, senescence, and inflammatory signals, as well as by enhancing ECM degradation. Future studies will establish the in vivo relevance of MSC priming to fibrosis resolution
Published in
Cytokine priming enhances the antifibrotic effects of human adipose derived mesenchymal stromal cells conditioned medium
Brizio M, Mancini M, Lora M et al. · Stem cell research & therapy 2024 · PMID 39334258 · doi:10.1186/s13287-024-03916-9
This dataset
Open GSE266052 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 GSE266052_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 PRJNA1105607 and SRA study SRP504478. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39334258) ↗
Study design
5 × Fibroblasts, Non-treated, vs 5 × Fibroblasts, TGF-β 72h, Non-treated 72h, vs 5 × Fibroblasts, TGF-β 72h, Resting hMSC(AT)-CM 72h, vs 5 × Fibroblasts, TGF-β 72h, Cytokine-primed hMSC(AT)-CM 72h,

Supports a between-group comparison across 20 samples.

How we read this: 4 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
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