Basic Study
Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 7, 2017; 23(1): 76-86
Published online Jan 7, 2017. doi: 10.3748/wjg.v23.i1.76
miRNA-133a-UCP2 pathway regulates inflammatory bowel disease progress by influencing inflammation, oxidative stress and energy metabolism
Xi Jin, Dong Chen, Ruo-Heng Zheng, Hong Zhang, Yi-Peng Chen, Zun Xiang
Xi Jin, Hong Zhang, Yi-Peng Chen, Zun Xiang, Department of Gastroenterology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, Zhejiang Province, China
Dong Chen, Department of Colorectal Surgery, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, Zhejiang Province, China
Ruo-Heng Zheng, Department of Clinical Medicine, Hangzhou Medical College, Hangzhou 310053, Zhejiang Province, China
Author contributions: Jin X and Chen D contributed equally as co-first authors; Jin X and Chen D performed the majority of experiments; Zheng RH, Zhang H and Chen YP performed the qRT-PCR, Western blot, RNAi, and data analysis and participated in the establishment of the animal model; Xiang Z designed the study and wrote the manuscript.
Supported by National Natural Science Foundation of China, No. 81370008 and No. 81000169; and Natural Science Foundation of Zhejiang Province, No. R2110159, No. LY15H030006 and No. LY16H030003.
Institutional review board statement: This study was carried out in accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health.
Institutional animal care and use committee statement: The protocol on animal was approved by the institutional review board of the First Affiliated Hospital of Zhejiang University.
Conflict-of-interest statement: There are no conflicts of interest or commercial financial support for this manuscript. The funding sources had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Data sharing statement: There is no other date elsewhere.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Zun Xiang, PhD, Department of Gastroenterology, The First Affiliated Hospital, School of Medicine, Zhejiang University, No. 79 Qingchun Road, Hangzhou 310003, Zhejiang Province, China. jxfl007@zju.edu.cn
Telephone: +86-571-87236611 Fax: +86-571-87236611
Received: September 5, 2016
Peer-review started: September 6, 2016
First decision: September 28, 2016
Revised: October 9, 2016
Accepted: November 15, 2016
Article in press: November 16, 2016
Published online: January 7, 2017
Processing time: 121 Days and 16.7 Hours
Core Tip

Core tip: The pathogenesis of inflammatory bowel disease (IBD) is unclear, but increasing evidence supports the involvement of epigenetic regulation such as the formation of miRNA-mRNA pairs. In this study, we investigated the role of the miR-133a-UCP2 pathway in the pathogenesis of IBD in a well-established mouse model. We found that the severity of IBD was alleviated after the UCP2 and miR-133a levels were antagonized and that the underlying mechanism may involve changes in inflammation, oxidative stress and energy metabolism. Our data provide novel clues and potential therapeutic targets for IBD.