Journal
CELL REPORTS
Volume 22, Issue 7, Pages 1810-1823Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.01.058
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Funding
- NIH [R35GM119787, R00CA178091, R01CA205420, P30CA023168]
- Jim and Diann Robbers Cancer Research Grant for New Investigators
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MicroRNA-223 is known as a myeloid-enriched anti-inflammatory microRNA that is dysregulated in numerous inflammatory conditions. Here, we report that neutrophilic inflammation (wound response) is augmented in miR-223-deficient zebrafish, due primarily to elevated activation of the canonical nuclear factor kB (NF-kappa B) pathway. NF-kappa B over-activation is restricted to the basal layer of the surface epithelium, although miR-223 is detected throughout the epithelium and in phagocytes. Not only phagocytes but also epithelial cells are involved in miR-223-mediated regulation of neutrophils' wound response and NF-kappa B activation. Cul1a/b, Traf6, and Tab1 are identified as direct targets of miR-223, and their levels rise in injured epithelium lacking miR-223. In addition, miR-223 is expressed in cultured human bronchial epithelial cells, where it also downregulates NF-kappa B signaling. Together, this direct connection between miR-223 and the canonical NF-kappa B pathway provides a mechanistic understanding of the multi-faceted role of miR-223 and highlights the relevance of epithelial cells in dampening neutrophil activation.
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