Abstract
Tight junction proteins play crucial roles in maintaining the integrity of intestinal mucosal barrier. MiRNA-182-5p is capable of targeting claudin-2 which is one of the vital tight junction proteins and the effect and mechanism of miRNA-182-5p was explored here in the DSS-induced colitis model. The pathological conditions were evaluated via hematoxylin and eosin staining. The gene expression level was assessed via PCR. Quantitative immunohistochemistry analysis was performed for the measurement of claudin-2. microRNA.org online tool was used for target gene prediction. Luciferase reporter assay and RNA pull-down assay were performed to detect the target of miRNA-182-5p. The inflammatory and oxidative stress level were measured using corresponding kits. MiRNA-182-5p was highly expressed in colitis model and miRNA-182-5p inhibitor exerted protective effects on colitis induced by DSS in mice. The protective effects includded improvement of pathological changes, increases in anti-inflammation and anti-oxidative genes, and up-regulation of TGF-β1. Claudin-2 mRNA was predicted as the target of miRNA-182-5p, which was validated via luciferase reporter assay and RNA pull-down assay. Claudin-2 overexpression was found in miRNA-182-5p inhibitor group. Consistent with the role of miRNA-182-5p, claudin-2 overexpression also exerted protective effects on DSS-induced colitis in mice. Inhibition of miRNA-182-5p exerted protective effects on colitis via targeting and upregulating claudin-2. The findings in study provide a new therapeutic strategy for colitis treatment and lay the foundation for future study.
Highlights
Inflammatory bowel disease is a refractory, nonspecific, debilitating inflammatory disease [1]
The mice in the study groups were sacrificed via euthanasia
All the findings suggested that silencing miRNA-182-5p protected against colonic injuries via targeting claudin-2
Summary
Inflammatory bowel disease is a refractory, nonspecific, debilitating inflammatory disease [1]. Ulcerative colitis and Crohn’s disease are two major forms of inflammatory bowel disease [2]. Common clinical manifestations include abdominal pain, fever, diarrhea, hematochezia, tenesmus, vomiting, and an increase in frequency of defecation [3, 4]. The incidence of inflammatory bowel disease is soaring globally [5,6,7]. Chronic colorectal inflammation has been confirmed as the vital contributor of tumorigenesis [8].
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