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01.01.2013 | Original Article—Alimentary Tract | Ausgabe 1/2013

Journal of Gastroenterology 1/2013

MicroRNA-146a negatively regulates PTGS2 expression induced by Helicobacter pylori in human gastric epithelial cells

Zeitschrift:
Journal of Gastroenterology > Ausgabe 1/2013
Autoren:
Zhen Liu, Di Wang, Yongliang Hu, Guoyong Zhou, Chaohui Zhu, Qi Yu, Yingchun Chi, Yingli Cao, Chiyu Jia, Quanming Zou
Wichtige Hinweise
Z. Liu, D. Wang, and Y. Hu contributed equally to this work.

Abstract

Background

Helicobacter pylori is a major human pathogenic bacterium in the gastric mucosa, but to date the regulatory mechanism of the H. pylori-induced inflammatory response is not clear. MicroRNAs have recently emerged as key post-transcriptional regulators of gene expression. We have previously reported that miR-146a negatively regulates the H. pylori-induced inflammatory response, but its molecular mechanism is just beginning to be explored. Our aim was to further explore the key targets of miR-146a and its role of regulation in H. pylori infection.

Methods

The potential targets of miR-146a were screened through bioinformatic approaches and identified by luciferase reporter assays and green fluorescent protein (GFP) repression experiments. Overexpression and inhibition of miR-146a were used to examine the impacts of miR-146a on its target gene, determined by quantitative real-time polymerase chain reaction (PCR) and western blotting.

Results

Prostaglandin endoperoxide synthase 2 (PTGS2) is a target gene of miR-146a, and miR-146a decreased PTGS2 expression by degradation of its mRNA, suggesting that the miR-146a-mediated inhibition is a post-transcriptional event. Furthermore, miR-146a and PTGS2 were significantly increased in H. pylori -infected human gastric epithelial cells. Overexpression of miR-146a resulted in significantly reduced PTGS2 production induced by H. pylori infection.

Conclusions

These results suggest that miR-146a may be involved in negatively regulating H. pylori-induced PTGS2 expression in human gastric epithelial cells.

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