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- Title
MicroRNA-155-enhanced Autophagy in Human Gastric Epithelial Cell in Response to Helicobacter Pylori.
- Authors
Kai Wu; Chaohui Zhu; Yi Yao; Xin Wang; Jiugang Song; Junshan Zhai
- Abstract
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.
- Subjects
AUTOPHAGY; EPITHELIAL cells; GASTRIC mucosa; GENE expression; HELICOBACTER diseases; HELICOBACTER pylori; IMMUNOHISTOCHEMISTRY; METAPLASIA
- Publication
Saudi Journal of Gastroenterology, 2016, Vol 22, Issue 1, p30
- ISSN
1319-3767
- Publication type
Article
- DOI
10.4103/1319-3767.173756