Basic Study
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. May 28, 2016; 22(20): 4881-4890
Published online May 28, 2016. doi: 10.3748/wjg.v22.i20.4881
miR-29a up-regulation in AR42J cells contributes to apoptosis via targeting TNFRSF1A gene
Qiang Fu, Tao Qin, Lin Chen, Chuan-Jiang Liu, Xu Zhang, Yu-Zhu Wang, Ming-Xing Hu, Hao-Yuan Chu, Hong-Wei Zhang
Qiang Fu, Tao Qin, Lin Chen, Chuan-Jiang Liu, Xu Zhang, Yu-Zhu Wang, Ming-Xing Hu, Hao-Yuan Chu, Hong-Wei Zhang, Department of Hepatobiliary Pancreatic Surgery, People’s Hospital of Zhengzhou University, School of Medicine, Zhengzhou University, Zhengzhou 450003, Henan Province, China
Author contributions: Fu Q and Chen L performed the majority of experiments; Qin T and Zhang HW designed the research and provided financial support for this work; Liu CJ conducted the experimental analysis; Wang YZ and Hu MX provided vital reagents and were involved in editing the manuscript; Zhang X and Chu HY analyzed sequencing data and developed analysis tools; Fu Q, Qin T and Chen L wrote the paper.
Institutional review board statement: This study was reviewed and approved by the Ethics Committee of People’s Hospital of Zhengzhou University.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Ethics Committee of People’s Hospital of Zhengzhou University.
Conflict-of-interest statement: We declare that we have no financial and personal relationships with other people or organizations that can inappropriately influence our work, and there is no professional or other personal interest of any nature or kind in any products, service and/ or company that could be construed as influencing the position presented in, or the review of, the manuscript entitled “miR-29a up-regulation in the AR42J cells contributes to apoptosis via targeting the TNFRSF1A gene”.
Data sharing statement: No additional data are available.
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: Hong-Wei Zhang, MD, PhD, Professor, Chief, Department of Hepatobiliary Pancreatic Surgery, People’s Hospital of Zhengzhou University, School of Medicine, Zhengzhou University, No. 7 Weiwu Road, Zhengzhou 450003, Henan Province, China. hwzhang666@126.com
Telephone: +86-371-65580368 Fax: +86-371-65580368
Received: January 8, 2016
Peer-review started: January 9, 2016
First decision: February 18, 2016
Revised: February 29, 2016
Accepted: March 18, 2016
Article in press: March 18, 2016
Published online: May 28, 2016
Core Tip

Core tip: Apoptosis is a self-protection mechanism in acute pancreatitis. miRNAs are short non-coding RNAs and play important roles in regulating gene expression in multiple cellular processes, such as apoptosis. Here, our group studied the role of miR-29a in pancreatic acinar cell apoptosis. The pancreatic acinar cells showed a tendency to apoptosis when the expression of miR-29a elevated, while the apoptosis rate exhibited the opposite trend by down-regulating the expression of miR-29a. Moreover, we found TNFRSF1A, which encode TNFR1 protein, was a target gene of miR-29a. Our results demonstrated that miR-29a could promote the apoptosis of pancreatic acinar cells via up-regulating the expression of TNFRSF1A gene in acute pancreatitis.