MiR-339 attenuates LPS-induced intestinal epithelial cells inflammatory responses and apoptosis by targeting TLR4
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Genes & Genomics https://doi.org/10.1007/s13258-020-00977-x
RESEARCH ARTICLE
MiR-339 attenuates LPS-induced intestinal epithelial cells inflammatory responses and apoptosis by targeting TLR4 Meiying Xie1 · Lina Zhang1 · Luoye Li1 · Minhuan Fan1 · Lianjie Hou2 Received: 21 December 2019 / Accepted: 22 July 2020 © The Genetics Society of Korea 2020
Abstract 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 miR339 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. Keywords MiR-339 · NF-κB · P53 · Inflammatory responses · Apoptosis
Introduction
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s13258-020-00977-x) contains supplementary material, which is available to authorized users. * Lianjie Hou [email protected] 1
Collaborative Innovation Center of Plant Pest Management and Bioenvironmental Health Application Technology, Guangdong Eco-Engineering Polytechnic, 297 Guangshan First Road, Tianhe District, Guangzhou 510520, Guangdong, China
Qingyuan City People’s Hospital, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan 511518, Guangdong, China
2
The intestinal epithelium is a single layer of cells organized into crypts and villi, known as the most rapidly self-renewing tissue in mammals. The cells that line the intestinal lumen perform the primary functions of digestion, water and nutrient absorption, and forms a
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