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©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Oct 21, 2020; 26(39): 5983-5996
Published online Oct 21, 2020. doi: 10.3748/wjg.v26.i39.5983
Published online Oct 21, 2020. doi: 10.3748/wjg.v26.i39.5983
Identification of differentially expressed genes in ulcerative colitis and verification in a colitis mouse model by bioinformatics analyses
Lei Shi, Yu Hao, Department of Immunology and Microbiology, School of Life Sciences, Beijing University of Chinese Medicine, Beijing 100029, China
Xiao Han, Jun-Xiang Li, Fu-Shun Kou, Zhi-Bin Wang, Rui Shi, Xing-Jie Zhao, Zhong-Mei Sun, Gastroenterology Department, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing 100078, China
Yu-Ting Liao, Department of Internal Medicine, Beijing Social Welfare Hospital, Beijing 100085, China
Author contributions: Shi L wrote the article and Han X edited it; Liao YT, Kou FS and Sun ZM performed the animal experiments; Wang ZB, Shi R and Zhao XJ analyzed the bioinformatics data; Hao Y and Li JX conducted the study.
Supported by Chinese Medicine Inheritance and Innovation “One Hundred Million” Talent Project Qihuang Scholar (to Li JX) ; The National Key R&D Program of China during the 13th Five-Year Plan Period , No. 2018YFC1705405 ; and The 66th China Postdoctoral Science Foundation , No. 2019M660575 .
Institutional review board statement: The data of ulcerative colitis we analyzed in this study were all from the National Center for Biotechnology Information-Gene Expression Omnibus database. According to the guidelines approved by the National Center for Biotechnology Information-Gene Expression Omnibus, our study did not require the separate ethics committee approval.
Institutional animal care and use committee statement: We complied with the ethics standard for research activity established by the Animal Ethics Committee of Beijing University of Chinese Medicine in accordance with the guidelines issued by the Regulations of Beijing Laboratory Animal Management.
Conflict-of-interest statement: The authors declare that they have no conflicts of interest.
Data sharing statement: Database we used in this study can be shared from the National Center for Biotechnology Information-Gene Expression Omnibus databases.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (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/
Corresponding author: Yu Hao, PhD, Professor, Department of Immunology and Microbiology, School of Life Sciences, Beijing University of Chinese Medicine, No. 11 North Third Ring East Road, Chaoyang District, Beijing 100029, China. yuhao64@sina.com
Received: June 10, 2020
Peer-review started: June 10, 2020
First decision: August 22, 2020
Revised: August 30, 2020
Accepted: September 16, 2020
Article in press: September 16, 2020
Published online: October 21, 2020
Peer-review started: June 10, 2020
First decision: August 22, 2020
Revised: August 30, 2020
Accepted: September 16, 2020
Article in press: September 16, 2020
Published online: October 21, 2020
Core Tip
Core Tip: Two microarray datasets were used, and differentially expressed genes were analyzed. Seventeen core genes were upregulated, and one was downregulated. These genes were markedly enriched in the cytokine-cytokine receptor interaction and chemokine signaling pathways. The top three core genes [C-X-C motif chemokine ligand 13, neuropeptide Y receptor Y1, C-X-C motif chemokine receptor 2 (CXCR2)] were verified in a dextran sulfate sodium-induced colitis model mice by real-time polymerase chain reaction and showed an increased expression, but only CXCR2 was statistically different. CXCR2 may represent a new biomarker to determine the degree of inflammation or a treatment target in ulcerative colitis.