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KMID : 0381120200420091097
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Genes and Genomics
2020 Volume.42 No. 9 p.1097 ~ p.1105
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MiR-339 attenuates LPS-induced intestinal epithelial cells inflammatory responses and apoptosis by targeting TLR4
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Xie Meiying
Zhang Lina
Li Luoye
Fan Minhuan
Hou Lianjie
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Abstract
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Background: Intestinal epithelial cells are important for defending against pathogen infection. LPS is an endotoxin that is highly antigenic and cytotoxic produced by bacteria. LPS disrupts the intestine epithelium integrity and induced the intestinal epithelial cell inflammation and apoptosis. Our previous study has predicted the function of exosome miRNAs through bioinformatics analysis, and we found that miR-339 had a potential function in cell inflammation response. To our knowledge, no published paper has demonstrated the miR-339 function in protecting the intestine epithelium against bacterial infection.
Objective: The objective of this study is to evaluate the miR-339 function in regulating intestinal epithelial cells to defend against bacterial infection through biological experiments and bioinformatics analyses.
Methods: Through the miR-339 transfection experiment and TLR4 interfering experiment, we evaluated the function of miR-339 and TLR4 in the process of inflammatory responses and apoptosis. Through Bioinformatics analyses and dual-luciferase reporter experiment, we identified the target gene of miR-339.
Results: miR-339 attenuates LPS-induced intestinal epithelial cells inflammatory responses through the TLR4/NF-κB signaling pathway and inhibited LPS-induced apoptosis through the P53 signaling pathway. TLR4 is the target gene of miR-339. TLR4 reduced LPS-induced proinflammatory responses and apoptosis.
Conclusions: In conclusion, miR-339 protected the intestine epithelial cells from LPS-induced cell inflammation and apoptosis through targeting TLR4. This study expanded our understanding of how miRNAs and genes work collaboratively in regulating intestinal epithelial cells to defend against bacterial infection.
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KEYWORD
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MiR-339, NF-κB, P53, Inflammatory responses, Apoptosis
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