Wenchao Yu1, Min Zhang2, Xin Li3, Ning Pan2, Xia Bian4, Wei Wu5. 1. Department of Intensive Care Unit, Dongying District People's Hospital, Dongying City, Shandong Province, People's Republic of China. 2. Department of Emergency, Shengli Oilfield Central Hospital, Dongying City, Shandong Province, People's Republic of China. 3. Department of Surgery, Dongying Shengli Shengcai Hospital, Dongying City, Shandong Province, People's Republic of China. 4. Dongying Medical Emergency Command Center, Dongying City, Shandong Province, People's Republic of China. 5. Department of Emergency, Dongying District People's Hospital, No.333 Jinan Road, Dongying District, Dongying City, 257000, Shandong Province, People's Republic of China. ckpwjs@163.com.
Abstract
BACKGROUND: Acute pancreatitis is a common inflammatory disease. MicroRNAs have been implicated in the pathogenesis of acute pancreatitis. AIMS: The purpose of this study was to investigate the precise roles of miR-193a-5p and miR-320-5p in AP. METHODS: The levels of miR-193a-5p, miR-320-5p and tumor necrosis factor receptor-associated factor 3 were detected by quantitative real-time polymerase chain reaction. Cell apoptosis was determined using flow cytometry. Enzyme-linked immunosorbent assay was performed to measure TNF-α, IL-6, IL-1β and IL-8 production, amylase activity, and malondialdehyde content. Targeted relationship between miR-193a-5p or miR-320-5p and TRAF3 was confirmed by the dual-luciferase reporter and RNA immunoprecipitation assays. RESULTS: Our data showed that miR-193a-5p and miR-320-5p were down-regulated in acute pancreatitis serum and caerulein-treated AR42J cells. The increased expression of miR-193a-5p or miR-320-5p alleviated caerulein-induced cell injury in AR42J cells. Tumor necrosis factor receptor-associated factor 3 was a direct target of miR-193a-5p and miR-320-5p in AR42J cells. Moreover, miR-193a-5p and miR-320-5p regulated caerulein-induced AR42J cells injury through targeting tumor necrosis factor receptor-associated factor 3. CONCLUSION: The present findings demonstrated that miR-193a-5p and miR-320-5p protected AR42J cells against caerulein-induced cell injury by targeting tumor necrosis factor receptor-associated factor 3, highlighting their roles as potential therapeutic targets for acute pancreatitis treatment.
BACKGROUND: Acute pancreatitis is a common inflammatory disease. MicroRNAs have been implicated in the pathogenesis of acute pancreatitis. AIMS: The purpose of this study was to investigate the precise roles of miR-193a-5p and miR-320-5p in AP. METHODS: The levels of miR-193a-5p, miR-320-5p and tumor necrosis factor receptor-associated factor 3 were detected by quantitative real-time polymerase chain reaction. Cell apoptosis was determined using flow cytometry. Enzyme-linked immunosorbent assay was performed to measure TNF-α, IL-6, IL-1β and IL-8 production, amylase activity, and malondialdehyde content. Targeted relationship between miR-193a-5p or miR-320-5p and TRAF3 was confirmed by the dual-luciferase reporter and RNA immunoprecipitation assays. RESULTS: Our data showed that miR-193a-5p and miR-320-5p were down-regulated in acute pancreatitis serum and caerulein-treated AR42J cells. The increased expression of miR-193a-5p or miR-320-5p alleviated caerulein-induced cell injury in AR42J cells. Tumor necrosis factor receptor-associated factor 3 was a direct target of miR-193a-5p and miR-320-5p in AR42J cells. Moreover, miR-193a-5p and miR-320-5p regulated caerulein-induced AR42J cells injury through targeting tumor necrosis factor receptor-associated factor 3. CONCLUSION: The present findings demonstrated that miR-193a-5p and miR-320-5p protected AR42J cells against caerulein-induced cell injury by targeting tumor necrosis factor receptor-associated factor 3, highlighting their roles as potential therapeutic targets for acute pancreatitis treatment.
Authors: Cherie Blenkiron; Kathryn J Askelund; Satyanarayan T Shanbhag; Mandira Chakraborty; Maxim S Petrov; Brett Delahunt; John A Windsor; Anthony R Phillips Journal: Ann Surg Date: 2014-08 Impact factor: 12.969
Authors: Sven M van Dijk; Nora D L Hallensleben; Hjalmar C van Santvoort; Paul Fockens; Harry van Goor; Marco J Bruno; Marc G Besselink Journal: Gut Date: 2017-08-24 Impact factor: 23.059