Saudi Journal of Gastroenterology
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ORIGINAL ARTICLE
Year : 2016  |  Volume : 22  |  Issue : 1  |  Page : 30-36

MicroRNA-155-enhanced autophagy in human gastric epithelial cell in response to Helicobacter pylori


Department of Gastroenterology, 309 Hospital of Chinese Peoples Liberation Army, Beijing, China

Correspondence Address:
Dr. Kai Wu
Department of Gastroenterology, 309 Hospital of Chinese Peoples Liberation Army, Beijing - 100 091
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1319-3767.173756

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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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