ArticleHuman cell2026
Bone marrow mesenchymal stem cell-derived exosomes exert therapeutic effects on inflammatory bowel disease through miR-148a-3p/Ets-1-dependent inhibition of pyroptosis.
Article in Human cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Inflammatory bowel disease (IBD) is a non-specific chronic inflammatory condition of the gastrointestinal tract, characterized by damage to intestinal epithelial cells (IECs) and inflammation. Mesenchymal stem cell-derived exosomes show therapeutic potential in IBD, but the underlying mechanisms remain unclear. This study investigates the therapeutic potential of bone marrow mesenchymal stem cell (BMSC)-derived exosomes and their molecular mechanism in IBD. We isolated and characterized exosomes from mouse BMSCs, confirming their typical size, morphology, and marker expression. In a dextran sulfate sodium (DSS)-induced mouse IBD model, administration of BMSC-derived exosomes alleviated disease severity, colon shortening, and histopathological damage. In LPS + ATP-stimulated IECs, BMSC-exos upregulated miR-148a-3p expression, enhanced cell viability, and suppressed pyroptosis-related proteins, including NOD-like receptor protein 3 (NLRP3), ASC, cleaved caspase-1, and the N-terminus of GSDMD (GSDMD-N), and inflammatory cytokines interleukin 1β (IL-1β), IL-18, tumor necrosis factor-α (TNF-α), and IL-6. Bioinformatics and dual-luciferase reporter assays identified E26 avian leukemia oncogene 1, 5' domain (Ets-1) as a direct target of miR-148a-3p. Ets-1 knockdown reversed the effects of miR-148a-3p inhibition on IEC pyroptosis and inflammation. In conclusion, BMSC-derived exosomes deliver miR-148a-3p to IECs, where it targets Ets-1 to suppress cellular pyroptosis and inflammatory responses, offering a novel therapeutic strategy for IBD.
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