Bao Yin1, Huang Tian-Chu2, Xu Ling-Fen3. 1. Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China; Department of Rehabilitation, Shengjing Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China. 2. Key Laboratory of Congenital Malformation, Ministry of Health, Shengjing Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China. 3. Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China.
Abstract
BACKGROUND: Increasing evidence shows that microRNA-7a-5p (miR-7a-5p) plays an important role in regulating the inflammatory process in inflammatory bowel disease (IBD). How miR-7a-5p contributes to this process is poorly defined. The purpose of this study was to examine whether miR-7a-5p regulates 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced inflammatory responses via the JNK pathway. METHODS: Colitis was induced in male mice by intracolonic administration of TNBS; mice were divided into 3 groups: normal control (NC), TNBS, and miR-7a-5p antagomir-treated group. Inflammatory responses were estimated by disease activity index (DAI) and histological scores. The relative expressions of miR-7a-5p and tight junction protein, ZO-1, were detected by RT-qPCR. Western blot assays were used to estimate the level of JNK pathway proteins and ZO-1. After miRNA-antagomir injection, the extent of colonic tissue injury and expression levels of ZO-1 and JNK in intestinal tissue were compared. RESULTS: miR-7a-5p and p-JNK expression were higher in the intestinal tissue of the TNBS group as compared to NC. Inhibition of the expression of miR-7a-5p resulted in significantly decreased expression of p-JNK but increased expression of ZO-1 and promoted the recovery of intestinal mucosa. CONCLUSION: This work demonstrates a correlation between the JNK pathway and miR-7a-5p in TNBS-induced experimental colitis in mice, which may provide a new research direction for the treatment of IBD.
BACKGROUND: Increasing evidence shows that microRNA-7a-5p (miR-7a-5p) plays an important role in regulating the inflammatory process in inflammatory bowel disease (IBD). How miR-7a-5p contributes to this process is poorly defined. The purpose of this study was to examine whether miR-7a-5p regulates 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced inflammatory responses via the JNK pathway. METHODS: Colitis was induced in male mice by intracolonic administration of TNBS; mice were divided into 3 groups: normal control (NC), TNBS, and miR-7a-5p antagomir-treated group. Inflammatory responses were estimated by disease activity index (DAI) and histological scores. The relative expressions of miR-7a-5p and tight junction protein, ZO-1, were detected by RT-qPCR. Western blot assays were used to estimate the level of JNK pathway proteins and ZO-1. After miRNA-antagomir injection, the extent of colonic tissue injury and expression levels of ZO-1 and JNK in intestinal tissue were compared. RESULTS: miR-7a-5p and p-JNK expression were higher in the intestinal tissue of the TNBS group as compared to NC. Inhibition of the expression of miR-7a-5p resulted in significantly decreased expression of p-JNK but increased expression of ZO-1 and promoted the recovery of intestinal mucosa. CONCLUSION: This work demonstrates a correlation between the JNK pathway and miR-7a-5p in TNBS-induced experimental colitis in mice, which may provide a new research direction for the treatment of IBD.
Authors: Kirstin Reinecke; Sevgi Eminel; Franziska Dierck; Wibke Roessner; Sabine Kersting; Ansgar Michael Chromik; Olga Gavrilova; Ale Laukevicience; Ivo Leuschner; Vicki Waetzig; Philip Rosenstiel; Thomas Herdegen; Christian Sina Journal: PLoS One Date: 2012-03-13 Impact factor: 3.240