MiR-34c and PlncRNA1 mediated the function of intestinal epithelial barrier by regulating tight junction proteins in inflammatory bowel disease.

BACKGROUND:Inflammatory bowel disease (IBD) is originated from uncontrolled inflammation, and desired methods for IBD therapy remains the main difficult. The network comprised with miRNA and lncRNA has been verified to play an important role on diverse human diseases. In this study, we demonstrated the role of miR-34c and lncRNA PlncRNA1 on the function of intestinal barrier. METHODS:Intestinal epithelial barrier model was constructed based on normal intestinal epithelial cell line Caco-2. 2% DSS was supplemented in the Apical side of the model cells to induce the injury of intestinal epithelial barrier. or western blot was used to determine mRNA or protein expression of miR-34c, PlncRNA1, Myc-associated zinc finger protein (MAZ), zonula occludens 1 (ZO-1) and occludin. RESULTS:DSS induced injury of intestinal epithelial barrier, while overexpression of PlncRNA1 seemed to protect intestinal epithelial barrier from injury. Tight junction (TJ) proteins ZO-1 and occludin were regulated by MAZ, while, miR-34c targeted MAZ to regulate its expression, in addition, PlncRNA1 and miR-34c bound together to regulate the expressions of MAZ, ZO-1 and occludin. The protect effects of PlncRNA1 overexpression on intestinal epithelial barrier function was reversed by overexpression of miR-34c. CONCLUSION:MAZ and TJ proteins were involved in the function of intestinal epithelial barrier, while miR-34c and PlncRNA1 regulated the intestinal dysfunction cooperatively.

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