Basic Study
Copyright ©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 14, 2021; 27(46): 7982-7994
Published online Dec 14, 2021. doi: 10.3748/wjg.v27.i46.7982
Recombinant protein Schistosoma japonicum-derived molecule attenuates dextran sulfate sodium-induced colitis by inhibiting miRNA-217-5p to alleviate apoptosis
Li-Chao Zhang, Xiao-Ying Wu, Rui-Bing Yang, Fang Chen, Jia-Hua Liu, Yun-Yi Hu, Zhong-Dao Wu, Li-Fu Wang, Xi Sun
Li-Chao Zhang, Rui-Bing Yang, Jia-Hua Liu, Yun-Yi Hu, Zhong-Dao Wu, Xi Sun, Department of Parasitology of Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510000, Guangdong Province, China
Xiao-Ying Wu, Department of Gastroenterology, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, Guangdong Province, China
Fang Chen, School of Medicine, South China University of Technology, South China University of Technology, Guangzhou 510000, Guangdong Province, China
Li-Fu Wang, Key Laboratory of Tropical Disease Control, Ministry of Education, Sun Yat-sen University, Guangzhou 510080, Guangdong Province, China
Author contributions: Sun X contributed to the experiment design; Wu ZD, Yang RB, and Chen F contributed to the experiment implementation; Liu JH and Hu YY analyzed the data; Zhang LC and Wang LF conceived the experiments, performed the experiments, and wrote the manuscript; all authors participated in critical revision of the manuscript and approved the final manuscript.
Supported by the National Natural Science Foundation of China, No. 81902081 and No. 81871682; the Natural Science Foundation of Guangdong Province, No. 2020A1515011573 and No. 2019A1515012068; China Postdoctoral Science Foundation, No. 2018M640858 and No. 2019T120771; Fundamental Research Funds for the Central Universities, No. 19ykpy170, No. 17ykpy09 and No. 19ykpy29; National Science and Technology Major Project, No. 2018ZX10101002-001; the 111 Project, No. B12003; and the Natural Science Foundation of Guangdong Province, No. 2021A1515010976.
Institutional review board statement: The study was reviewed and approved by the Sun Yat-sen University Institutional Review Board.(Approval No. SYSU-IACUC-2019-B517).
Conflict-of-interest statement: The authors declare no competing interests.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: I 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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Li-Fu Wang, DO, Research Scientist, Key Laboratory of Tropical Disease Control, Ministry of Education, Sun Yat-sen University, No. 74 Zhongshan Road, Guangzhou 510080, Guangdong Province, China. wanglf99999@163.com
Received: June 16, 2021
Peer-review started: June 16, 2021
First decision: June 30, 2021
Revised: July 9, 2021
Accepted: November 29, 2021
Article in press: November 29, 2021
Published online: December 14, 2021
Core Tip

Core Tip: The lack of therapeutic targets has limited the treatment of inflammatory bowel disease (IBD). Parasitic nematode infections can ameliorate clinical and experimental colitis. Our previous study found that rSj16, a 16-kDa secreted protein of Schistosoma japonicum produced by Escherichia coli, has protective effects on dextran sulfate sodium (DSS)-induced colitis in mice. We found that rSj16 can inhibit DSS-induced apoptosis in the colons of mice with colitis. In addition, we found that the inhibitory effect of rSj16 on apoptosis was associated with decreased miR-217-5p, and that hepatocyte nuclear factor 1 beta was increased after treatment with rSj16. These results highlight a novel therapeutic target that may be used to treat IBD.