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MicroRNA-155-enhanced Autophagy in Human Gastric Epithelial Cell in Response to Helicobacter Pylori

BACKGROUND/AIM: MicroRNAs (miRNAs) are a class of small noncoding RNAs acting as posttranscriptional gene expression regulators in many physiological and pathological conditions. MiR-155 is one kind of miRNAs that plays an important role in causing various diseases. However, the precise molecular me...

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Autores principales: Wu, Kai, Zhu, Chaohui, Yao, Yi, Wang, Xin, Song, Jiugang, Zhai, Junshan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4763526/
https://www.ncbi.nlm.nih.gov/pubmed/26831604
http://dx.doi.org/10.4103/1319-3767.173756
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author Wu, Kai
Zhu, Chaohui
Yao, Yi
Wang, Xin
Song, Jiugang
Zhai, Junshan
author_facet Wu, Kai
Zhu, Chaohui
Yao, Yi
Wang, Xin
Song, Jiugang
Zhai, Junshan
author_sort Wu, Kai
collection PubMed
description BACKGROUND/AIM: MicroRNAs (miRNAs) are a class of small noncoding RNAs acting as posttranscriptional gene expression regulators in many physiological and pathological conditions. MiR-155 is one kind of miRNAs that plays an important role in causing various diseases. However, the precise molecular mechanism of the ectopic expression of miR-155 in Helicobacter pylori infection remains poorly understood. Autophagy has recently been identified as an effective way to control the intracellular bacterium survival. In the present study, we demonstrate a novel role of miR-155 in regulating the autophagy-mediated anti-H. pylori response. PATIENTS AND METHODS: Totally 86 H. pylori-positive patients together with 10 H. pylori-negative, healthy control subjects were included in the study. Correlation between immunohistochemical grades and miR-155 expression were determined. Molecular mechanism of miR-155 on regulation of autophagy and elimination of intracellular H. pylori were determined using the GES-1 cell model. RESULTS: We found that overexpression of miR-155 by transfecting miR-155 mimics could significantly decrease the survival of intracellular H. pylori, and this process was through induction of autophagy. Furthermore, there was a significant correlation between miR-155 and immunohistochemical grades in H. pylori-positive patients, and miR-155 expression were decreased in the intestinal metaplasia group. CONCLUSIONS: The results have indicated that the miR-155 expression level plays a key role in immunity response against H. pylori and this might provide potential targets for the future treatment of H. pylori-related diseases.
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spelling pubmed-47635262016-03-07 MicroRNA-155-enhanced Autophagy in Human Gastric Epithelial Cell in Response to Helicobacter Pylori Wu, Kai Zhu, Chaohui Yao, Yi Wang, Xin Song, Jiugang Zhai, Junshan Saudi J Gastroenterol Original Article BACKGROUND/AIM: MicroRNAs (miRNAs) are a class of small noncoding RNAs acting as posttranscriptional gene expression regulators in many physiological and pathological conditions. MiR-155 is one kind of miRNAs that plays an important role in causing various diseases. However, the precise molecular mechanism of the ectopic expression of miR-155 in Helicobacter pylori infection remains poorly understood. Autophagy has recently been identified as an effective way to control the intracellular bacterium survival. In the present study, we demonstrate a novel role of miR-155 in regulating the autophagy-mediated anti-H. pylori response. PATIENTS AND METHODS: Totally 86 H. pylori-positive patients together with 10 H. pylori-negative, healthy control subjects were included in the study. Correlation between immunohistochemical grades and miR-155 expression were determined. Molecular mechanism of miR-155 on regulation of autophagy and elimination of intracellular H. pylori were determined using the GES-1 cell model. RESULTS: We found that overexpression of miR-155 by transfecting miR-155 mimics could significantly decrease the survival of intracellular H. pylori, and this process was through induction of autophagy. Furthermore, there was a significant correlation between miR-155 and immunohistochemical grades in H. pylori-positive patients, and miR-155 expression were decreased in the intestinal metaplasia group. CONCLUSIONS: The results have indicated that the miR-155 expression level plays a key role in immunity response against H. pylori and this might provide potential targets for the future treatment of H. pylori-related diseases. Medknow Publications & Media Pvt Ltd 2016 /pmc/articles/PMC4763526/ /pubmed/26831604 http://dx.doi.org/10.4103/1319-3767.173756 Text en Copyright: © 2016 Saudi Journal of Gastroenterology (Official journal of The Saudi Gastroenterology Association) http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.
spellingShingle Original Article
Wu, Kai
Zhu, Chaohui
Yao, Yi
Wang, Xin
Song, Jiugang
Zhai, Junshan
MicroRNA-155-enhanced Autophagy in Human Gastric Epithelial Cell in Response to Helicobacter Pylori
title MicroRNA-155-enhanced Autophagy in Human Gastric Epithelial Cell in Response to Helicobacter Pylori
title_full MicroRNA-155-enhanced Autophagy in Human Gastric Epithelial Cell in Response to Helicobacter Pylori
title_fullStr MicroRNA-155-enhanced Autophagy in Human Gastric Epithelial Cell in Response to Helicobacter Pylori
title_full_unstemmed MicroRNA-155-enhanced Autophagy in Human Gastric Epithelial Cell in Response to Helicobacter Pylori
title_short MicroRNA-155-enhanced Autophagy in Human Gastric Epithelial Cell in Response to Helicobacter Pylori
title_sort microrna-155-enhanced autophagy in human gastric epithelial cell in response to helicobacter pylori
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4763526/
https://www.ncbi.nlm.nih.gov/pubmed/26831604
http://dx.doi.org/10.4103/1319-3767.173756
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