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Regulation of Hematopoietic Inflammatory Signaling by MIRC11 and miR-146a

GSE335378 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2026/07/29 Platform GPL19057
Summary
Disruption of inflammatory pathways contributes to hematopoietic disorders such as leukemia, cytopenias, myelo-dysplastic syndromes (MDS), and myeloproliferative diseases (MPD). Although chronic inflammation impairs normal hematopoiesis, a low level of inflammatory signaling is essential for maintaining hematopoietic stem cell (HSC) homeostasis. Here, we report that mice lacking MiRNA Cluster 11 (Mirc11: encodes miR-23a, miR-24-2, and miR-27a) display reduced inflammatory signaling, including diminished IFN-α/β, IFN-γ, TNF, IL-6, and Toll-like receptor (TLR) pathway activity. Notably, this phenotype is opposite of that seen in miR146a-deficient mice, which exhibit hyperinflammation leading to bone marrow failure. These contrasting phenotypes suggest that Mirc11 miRNAs and miR-146a may function together to buffer inflammatory signaling and maintain immune homeostasis.
Published in
Balancing inflammatory signaling in hematopoiesis: roles of MIRC11 and miR-146a
Boucher AC, Payne TJ, Pulakanti K et al. · Frontiers in immunology 2026 · PMID 42488682 · doi:10.3389/fimmu.2026.1828453
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Also filed as BioProject PRJNA1478444 and SRA study SRP709574. Searching any of these in the dataset finder brings you back here.

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