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Macrophage Smad1 contributes to post-infarction dysfunction, suppressing angiogenic chemokine expression, and stimulating extracellular matrix remodeling

GSE288948 Mus musculus (mouse) RNA-seq (gene expression) 18 samples Submitted 2026/02/06 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 18 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
18 samples: 18 samples, each with a distinct title — no replicated groupsGroups 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)
In healing infarcts, macrophages undergo dramatic phenotypic changes in response to cytokines and growth factors and serve as central effectors in cardiac repair and remodeling. TGF-β superfamily members are key regulators of macrophages and signal predominantly through activation of Smad-dependent cascades. Although the involvement of TGF-β/Smad3 in regulation of macrophage phenotype has been documented, there is no information on the in vivo effects of macrophage Smad1 signaling.
Read the full summary ↓
To study the role of macrophage Smad1 in myocardial infarction, we performed in vitro studies and in vivo experiments using mice with myeloid cell-specific Smad1 loss. Macrophage Smad1 activation peaked 7 days after infarction. In vitro, TGF-β1, TGF-β3 and BMP6, but not by BMP2, BMP4 and BMP7, stimulated Smad1 activation. In vivo, myeloid cell-specific Smad1 loss attenuated post-infarction adverse remodeling and ventricular dysfunction, increasing angiogenesis and decreasing extracellular matrix denaturation. Acquisition of an angiogenic profile by macrophages in the absence of Smad1, involved upregulation of the angiogenic chemokine CXCL12. In conclusion, our findings demonstrate for the first time that macrophage Smad1 inhibits release of angiogenic chemokines and enhances expression of genes involved in extracellular matrix remodeling.
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 GSE288948_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: 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 PRJNA1220077. Searching any of these in the dataset finder brings you back here.

Study design
18 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 18 sample titles: 18 distinct titles with little repetition. 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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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.