MiR-155-5p Elevated by Ochratoxin A Induces Intestinal Fibrosis and Epithelial-to-Mesenchymal Transition through TGF-beta Regulated Signaling Pathway In Vitro and In Vivo

Ochratoxin A ( OTA) is a mycotoxin that induces fibrosis and epithelial-to-mesenchymal transitions (EMT) in kidneys and livers. It enters our bodies through food consumption, where it is absorbed in the intestines. However, the impact of OTA on the intestines is yet to be studied. MicroRNA (miRNAs) are small non-coding single-stranded RNAs that block the transcription of specific mRNAs and are, therefore, involved in many biochemical processes. Our findings indicate that OTA can induce EMT and intestinal fibrosis both in vivo and in vitro. This study examines the impact of OTA on intestinal toxicity and the role of miRNAs in this process. Following OTA treatment, miR-155-5p was the most elevated miRNA by next- generation sequencing. Our research showed that OTA increased miR-155-5p levels through transforming growth factor beta (TGF-beta), leading to the development of intestinal fibrosis and EMT. Additionally, the study identified that the modulation of TGF-beta and miR-155-5p by OTA is linked to the inhibition of CCAAT/enhancer-binding protein beta (C/EBP beta) and Smad2/3 accumulation in the progression of intestinal fibrosis.

Automated summary

This study explores the impact of Ochratoxin A (OTA) on intestinal toxicity and the role of microRNAs (miRNAs) in producing this effect. The findings suggest that OTA induces epithelial-to-mesenchymal transitions (EMT) and intestinal fibrosis. The research identifies miR-155-5p as the most elevated miRNA following OTA treatment, with OTA increasing miR-155-5p levels through transforming growth factor beta (TGF-beta), leading to the development of intestinal fibrosis and EMT.