Faculty, Staff and Student Publications

Language

English

Publication Date

10-22-2025

Journal

JCI Insight

DOI

10.1172/jci.insight.190466

PMID

40956617

PMCID

PMC12581662

PubMedCentral® Posted Date

9-16-2025

PubMedCentral® Full Text Version

Post-print

Abstract

The intestinal mucosal epithelium forms a barrier between luminal contents and the body. MicroRNAs (miRNAs) regulate mucosal homeostasis by controlling inflammatory responses and structural integrity. Here, we discovered a protective role for miR147 in intestinal inflammation using a miR147tdTomato reporter mouse. miR147 was enriched in the intestines, with the highest expression in the colonic epithelial cells at the luminal surface, with prominent expression in differentiated enterocytes. Mice with general or intestinal epithelial deletion of miR147 showed increased intestinal inflammation and diminished mucosal healing during colitis. RNA sequencing of miR147-deficient cells showed dysregulated immune signaling, with upregulated proinflammatory cytokine pathways and reduced type I interferon responses and revealed Ndufa4 as a likely miR147 target. Ndufa4, a mitochondrial protein regulating energy metabolism and inflammation, was elevated at the crypt base, inversely correlating with miR147. Mice lacking the miR147 binding site in Ndufa4's 3'-UTR phenocopied miR147-deficient mice during colitis. Spatial and single-cell transcriptomic analyses in murine and human colons showed mutually exclusive miR147 and Ndufa4 expression, consistent with a regulatory relationship in epithelial differentiation and metabolism. These findings underscore miR147's role in intestinal homeostasis and mucosal healing, suggesting it as a therapeutic target for inflammatory bowel disease.

Keywords

Animals, MicroRNAs, Intestinal Mucosa, Mice, Humans, Colitis, Inflammation, Disease Models, Animal, Mice, Inbred C57BL, Colon, Male, Mice, Knockout, Wound Healing

Published Open-Access

yes

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