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MiR-32-5p aggravates intestinal epithelial cell injury in pediatric enteritis induced by Helicobacter pylori.

Authors
  • Feng, Jing1
  • Guo, Jian2
  • Wang, Jun-Ping3
  • Chai, Bao-Feng4
  • 1 Institute of Loess Plateau, Shanxi University, Taiyuan 030006, Shanxi Province, China. , (China)
  • 2 Department of General Surgery, Shanxi Provincial People's Hospital, The Affiliated People's Hospital of Shanxi Medical University, Taiyuan 030012, Shanxi Province, China. , (China)
  • 3 Department of Gastroenterology, Shanxi Provincial People's Hospital, The Affiliated People's Hospital of Shanxi Medical University, Taiyuan 030012, Shanxi Province, China. , (China)
  • 4 Institute of Loess Plateau, Shanxi University, Taiyuan 030006, Shanxi Province, China. [email protected] , (China)
Type
Published Article
Journal
World journal of gastroenterology
Publication Date
Nov 07, 2019
Volume
25
Issue
41
Pages
6222–6237
Identifiers
DOI: 10.3748/wjg.v25.i41.6222
PMID: 31749593
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Pediatric enteritis is one of the infectious diseases in the digestive system that causes a variety of digestive problems, including diarrhea, vomiting, and bellyache in children. Clinically, Helicobacter pylori (H. pylori) infection is one of the common factors to cause pediatric enteritis. It has been demonstrated that aberrant expression of microRNAs (miRNAs) is found in gastrointestinal diseases caused by H. pylori, and we discovered a significant increase of miR-32-5p in H. pylori-related pediatric enteritis. However, the exact role of miR-32-5p in it is still unknown. To investigate the role of aberrant miR-32-5p in pediatric enteritis induced by H. pylori. MiR-32-5p expression was detected by quantitative real time-polymerase chain reaction. The biological role of miR-32-5p in H. pylori-treated intestinal epithelial cells was evaluated by Cell Counting Kit-8 assay and flow cytometry. The potential target of miR-32-5p was predicted with TargetScanHuman and verified by luciferase assay. The downstream mechanism of miR-32-5p was explored by using molecular biology methods. We found that miR-32-5p was overexpressed in serum of H. pylori-induced pediatric enteritis. Further investigation revealed that H. pylori infection promoted the death of intestinal epithelial cells, and increased miR-32-5p expression. Moreover, miR-32-5p mimic further facilitated apoptosis and inflammatory cytokine secretion of intestinal epithelial cells. Further exploration revealed that SMAD family member 6 (SMAD6) was the direct target of miR-32-5p, and SMAD6 overexpression partially rescued cell damage induced by H. pylori. The following experiments showed that miR-32-5p/SMAD6 participated in the apoptosis of intestinal epithelial cells induced by transforming growth factor-β-activated kinase 1 (TAK1)-p38 activation under H. pylori infection. Our work uncovered the crucial role of aberrant expression of miR-32-5p in H. pylori-related pediatric enteritis, and suggested that the TAK1-p38 pathway is involved in it. ©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.

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