Original Article
Copyright ©2013 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Dec 7, 2013; 19(45): 8282-8291
Published online Dec 7, 2013. doi: 10.3748/wjg.v19.i45.8282
Overexpressed miRNA-155 dysregulates intestinal epithelial apical junctional complex in severe acute pancreatitis
Rui Tian, Rui-Lan Wang, Hui Xie, Wei Jin, Kang-Long Yu
Rui Tian, Rui-Lan Wang, Hui Xie, Wei Jin, Kang-Long Yu, Intensive Care Unit, First People′s Hospital, Shanghai Jiaotong University, Shanghai 201620, China
Author contributions: Tian R designed the study, performed the majority of experiments, and wrote the manuscript; Wang R proposed the study concept, provided vital reagents and analytical tools, and reviewed the manuscript; Xie H, Jin W and Yu K were involved in the experimental work and data analysis.
Supported by The research grants from Shanghai Municipal Science and Technology Commission, No. 114119b2900 and Shanghai Municipal Key Laboratory of Pancreatic Disease, No. P2012006
Correspondence to: Rui-Lan Wang, MD, Intensive Care Unit, First People′s Hospital, Shanghai Jiaotong University, 650 Xin Songjiang Road, Shanghai 201620, China. wangyusun@hotmail.com
Telephone: +86-21-37798521 Fax: +86-21-37798521
Received: May 28, 2013
Revised: September 11, 2013
Accepted: September 29, 2013
Published online: December 7, 2013
Core Tip

Core tip: Apical junction complex (AJC) damage leads to intestinal barrier dysfunction and disease progression in severe acute pancreatitis (SAP) by an unknown mechanism. We reported for the first time that miRNA (miR)-155, a major mediator regulating early-stage inflammatory process, was overexpressed in experimental SAP intestinal epithelia as induced by circulating tumor necrosis factor (TNF)-α. RhoA gene, a predicted targeted gene for miR-155, was underexpressed at the post-transcriptional level, accompanied by downregulation of ZO-1 and E-cadherin expression; two key component proteins of AJC. Our study demonstrated that the TNF-α/miR-155/RhoA/ZO-1/E-cadherin signaling pathway contributed to intestinal barrier dysfunction in complicated SAP.