GEO series

Gas6-Axl signaling drives oral regenerative wound repair [RNA-Seq]

GSE287947 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2025/04/30 Platform GPL19057

Summary

Rapid and scarless wound repair is a hallmark of the oral mucosa, yet the cellular and molecular mechanisms that enable this regeneration remain unclear. By comparing populations of oral mucosal fibroblasts (OMFs) and facial skin fibroblasts (FSFs), we have identified the mechanisms that facilitate regeneration over fibrosis. We found that OMFs utilize Growth arrest specific-6 (GAS6)-AXL signaling to suppress fibrosis-related mechanosignaling via Focal adhesion kinase (FAK). Inhibition and knockdown of AXL in the oral mucosa resulted in fibrotic wounds and increased activation of FAK. At the same time, stimulation of AXL in the facial skin yielded wounds that heal regeneratively. Rare human oral scars that resulted from repetitive injury showed decreased expression of GAS6/AXL and increased FAK. Activating AXL in repetitively injured mouse oral tissue resulted in better wound healing outcomes and reduced scarring. Together, our work demonstrates that AXL signaling is necessary for regenerative wound healing in the oral mucosa and sufficient to limit facial skin fibrosis.

Published in

Growth arrest specific-6 and angiotoxin receptor-like signaling drive oral regenerative wound repair

Griffin MF, Cook J, Morgan A et al. · Science translational medicine 2025 · PMID 40601775 · doi:10.1126/scitranslmed.adk2101

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Direct links to NCBI, no account and no request form: the whole study as GSE287947_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 4 samples. Raw sequencing reads are also available from ENA.

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Also filed as BioProject PRJNA1215338 and SRA study SRP559778. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40601775) ↗

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