ArticleArchives of medical science : AMS2025
STAT1/MUC4 activation promotes antimicrobial peptide production to reduce intestinal epithelium barrier injury caused by enteropathogenic
Article in Archives of medical science : AMS, 2025. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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5 authors.
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Abstract
Introduction: Antimicrobial peptides (AMPs) are endogenous peptides that have been identified to alleviate intestinal epithelial barrier inflammation and dysfunction caused by enteropathogenic Material and methods: The binding of signal transducer and activator of transcription (STAT) 1 (STAT1) to mucin 4 (MUC4) was examined by co-immunoprecipitation assay. To detect the influence of STAT1 and MUC4 expression, a C57BL/6 mouse model of EPEC infection Results: p-STAT1, MUC4, ZO-1 and AMP-related genes were lowly expressed in the ileum of EPEC-infected mice. p-STAT1 and MUC4 bound to each other. The expression levels of STAT1 and MUC4 were decreased in EPEC-infected IEC. STAT1 overexpression counteracted the EPEC-induced reduction of viability, apoptosis promotion, ZO-1 activity inhibition, release of proinflammatory cytokines, and downregulation of MUC4 and AMP-related genes in IEC. MUC4 knockdown partly counteracted the effect of STAT1 overexpression, but did not affect the forced STAT1 overexpression in EPEC-infected IEC. Conclusions: STAT1/MUC4 pathway activation promotes AMP production to mitigate intestinal epithelium barrier injury caused by EPEC infection.
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