Abstract

BackgroundInflammatory bowel disease (IBD) is one of the chronic gastrointestinal diseases with increasing risk of colon cancer development in the future. Apoptosis and inflammation play an important role in the etiology of this disease. MicroRNAs are associated with etiology of different diseases including IBD. In this study, we aimed to explore the role of miR-135a in the etiology of colitis in murine model of DSS-induced colitis.ResultsThe results showed that expression of miR-135a in colonic cells was suppressed and up-regulating miR-135a inhibited apoptosis and inflammation of colonic epithelial cells. Additionally, Hif1α was identified as the target gene of miR-135a which promoted apoptosis and inflammation as knockdown of Hif1α led to the suppression of both apoptosis and inflammation.ConclusionsOverexpression of miR-135a might be beneficial in IBD due to its anti-apoptosis and anti-inflammation effects in vitro.

Highlights

  • Inflammatory bowel disease (IBD) is one of the chronic gastrointestinal diseases with increasing risk of colon cancer development in the future

  • Expression of miR-135a in dextran sodium sulfate (DSS)-induced colitis Our experimental results revealed that the mice was presented with symptoms of diarrhea and significant weight loss after 8 days of administration of 4% DSS

  • We have demonstrated that the expression of miR-135a was suppressed in the DSS-induced murine model of colitis and increased expression of miR-135a was associated with suppression of apoptosis and inflammation

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Summary

Introduction

Inflammatory bowel disease (IBD) is one of the chronic gastrointestinal diseases with increasing risk of colon cancer development in the future. Apoptosis and inflammation play an important role in the etiology of this disease. MicroRNAs are associated with etiology of different diseases including IBD. Inflammatory bowel disease (IBD) is a chronic condition which is characterized by inflammatory damage to small intestine and colon; the main IBD types include ulcerative colitis (UC) and Crohn’s disease (CD) [1]. Environmental factors play an important role in the etiology and progression of the disease [2]. IBD, especially UC (the risk is minimal with CD) is associated with increased risk of colon cancer [1, 2]

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