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Controlling Neuroinflammation
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
miRNAs are RNA molecules produced by the cells that negatively regulate gene expression by translational repression. miRNA binds to complementary sequences in mRNA, which either prevents translation or accelerates mRNA decay. miRNAs play key roles in cellular processes including virus–host interaction. Alterations in cellular miRNA expression may be an important determinant of virulence. When the pattern of expression of miRNAs was studied in the nervous system of mice infected with RABV attenuated ERA strain, it appears that expression of IRF3, STATS, TRIM25, and NFAT5 genes, the targets of up-regulated miRNAs miR-203, miR-290-3p, miR-207, and miR-1896, respectively, was down-regulated (Zhao et al. 2011 b). These data suggest that RABV infection could down-regulate inflammatory response through the production of miRNAs. Nevertheless, this study will require further confirmation using virulent RABV strains instead of attenuated strains.
Enterotoxigenic Bacteroides fragilis induces the stemness in colorectal cancer via upregulating histone demethylase JMJD2B
Published in Gut Microbes, 2020
Qian-Qian Liu, Chun-Min Li, Lin-Na Fu, Hao-Lian Wang, Juan Tan, Yun-Qian Wang, Dan-Feng Sun, Qin-Yan Gao, Ying-Xuan Chen, Jing-Yuan Fang
To explore the mechanism by which ETBF induces upregulation of JMJD2B at both the mRNA and protein levels, bioinformatic software was used to predict transcription factor binding sites at promoter regions of JMJD2B. We found that the JMJD2B promoter region contained multiple binding sites for NFAT5 (Supplementary Fig. S3A). NFAT5 is a transcription factor that functions as a cell signaling molecule involved in complex adaptive systems. Interaction of lipopolysaccharide (LPS) with host cells through TLRs upregulates the expression of NFAT5.36 Therefore, we hypothesized that dysregulated NFAT5 expression might contribute to ETBF-increased JMJD2B expression. Real-time PCR and western blotting revealed that exposure of HCT116 and DLD1 cells to ETBF, but not to NTBF, could dramatically increase the expression of NFAT5 (Figure 3A), whereas the mRNA levels of its isoforms, NFAT c1-c4, were not significantly affected in both HCT116 and DLD1 cells (Supplementary Fig. S3B). Further, we conducted luciferase reporter assays and found that forced overexpression of NFAT5 notably increased the luciferase activity of HCT116 and DLD1 cells transfected with a wild-type JMJD2B recombinant plasmid (JMJD2B-WT), but not with the mutant plasmid (JMJD2B-MT), which contains no binding sites for NFAT5 predicted by bioinformatic software (Figure 3B). These data indicated that NFAT5 could transcriptionally upregulate the expression of JMJD2B. Moreover, real-time PCR and western blotting revealed NFAT5 siRNA dramatically abrogated ETBF-induced upregulation of JMJD2B and NANOG (Figure 3C and Supplementary Fig. S3 C). In addition, sphere formation was reduced after knocking down NFAT5 in HCT116 and DLD1 cells co-cultured with ETBF, compared with that in the controls (Figure 3D). This effect was abolished in JMJD2B overexpression plasmid-transfected cells (Figure 3E, F).