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10.1097/MIB.0000000000000553 http://scihub22266oqcxt.onion/10.1097/MIB.0000000000000553 C4645954!4645954 !26332312     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26332312 &cmd=llinks): Failed to open stream: HTTP request failed! 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Microbial Disruption of Autophagy Alters Expression of the RISC Component AGO2, a Critical Regulator of the miRNA Silencing Pathway |pdf=|usr=}}{{26332312 }} gab.com Text Microbial Disruption of Autophagy Alters Expression of the RISC Component AGO2, a Critical Regulator of the miRNA Silencing Pathway JO: Inflamm Bowel Dis http://www.kidney.de/pget.php?&tw=1&pmid=26332312 #FOAvip BACKGROUND: Autophagy is implicated in Crohn's disease (CD) pathogenesis. Recent evidence suggests autophagy regulates the microRNA (miRNA)-induced silencing complex (miRISC). Therefore, autophagy may play a novel role in CD by regulating expression of miRISC, thereby altering miRNA silencing. As microbes associated with CD can alter autophagy, we hypothesized that microbial disruption of autophagy affects the critical miRISC component AGO2. METHODS: AGO2 expression was assessed in epithelial and immune cells, and intestinal organoids with disrupted autophagy. Microarray technology was used to determine the expression of downstream miRNAs in cells with defective autophagy. RESULTS: Increased AGO2 was detected in autophagy-deficient ATG5-/- and ATG16-/- mouse embryonic fibroblast cells (MEFs) in comparison with wild-type MEFs. Chemical agents and VacA toxin, which disrupt autophagy, increased AGO2 expression in MEFs, epithelial cells lines, and human monocytes, respectively. Increased AGO2 was also detected in ATG7-/- intestinal organoids, in comparison with wild-type organoids. Five miRNAs were differentially expressed in autophagy-deficient MEFs. Pathway enrichment analysis of the differentially expressed miRNAs implicated signaling pathways previously associated with CD. CONCLUSIONS: Taken together, our results suggest that autophagy is involved in the regulation of the critical miRISC component AGO2 in epithelial and immune cells and primary intestinal epithelial cells. We propose a mechanism by which autophagy alters miRNA expression, which likely impacts the regulation of CD-associated pathways. Furthermore, as enteric microbial products can manipulate autophagy and AGO2, our findings suggest a novel mechanism by which enteric microbes could influence miRNA to promote disease. Twit Text FOAVip Microbial Disruption of Autophagy Alters Expression of the RISC Component AGO2, a Critical Regulator of the miRNA Silencing Pathway ????Inflamm Bowel Dis http://www.kidney.de/pget.php?&tw=1&pmid=26332312 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26332312 #FOAvip English Wikipedia <ref>{{Cite pmid|26332312 }}</ref> Microbial Disruption of Autophagy Alters Expression of the RISC Component AGO2, a Critical Regulator of the miRNA Silencing Pathway #MMPMID26332312 Sibony M ; Abdullah M ; Greenfield L ; Raju D ; Wu T ; Rodrigues DM ; Galindo-Mata E ; Mascarenhas H ; Philpott DJ ; Silverberg MS ; Jones NL Inflamm Bowel Dis 2015[Dec]; 21 (12 ): 2778-86 PMID26332312 show ga BACKGROUND: Autophagy is implicated in Crohn's disease (CD) pathogenesis. Recent evidence suggests autophagy regulates the microRNA (miRNA)-induced silencing complex (miRISC). Therefore, autophagy may play a novel role in CD by regulating expression of miRISC, thereby altering miRNA silencing. As microbes associated with CD can alter autophagy, we hypothesized that microbial disruption of autophagy affects the critical miRISC component AGO2. METHODS: AGO2 expression was assessed in epithelial and immune cells, and intestinal organoids with disrupted autophagy. Microarray technology was used to determine the expression of downstream miRNAs in cells with defective autophagy. RESULTS: Increased AGO2 was detected in autophagy-deficient ATG5-/- and ATG16-/- mouse embryonic fibroblast cells (MEFs) in comparison with wild-type MEFs. Chemical agents and VacA toxin, which disrupt autophagy, increased AGO2 expression in MEFs, epithelial cells lines, and human monocytes, respectively. Increased AGO2 was also detected in ATG7-/- intestinal organoids, in comparison with wild-type organoids. Five miRNAs were differentially expressed in autophagy-deficient MEFs. Pathway enrichment analysis of the differentially expressed miRNAs implicated signaling pathways previously associated with CD. CONCLUSIONS: Taken together, our results suggest that autophagy is involved in the regulation of the critical miRISC component AGO2 in epithelial and immune cells and primary intestinal epithelial cells. We propose a mechanism by which autophagy alters miRNA expression, which likely impacts the regulation of CD-associated pathways. Furthermore, as enteric microbial products can manipulate autophagy and AGO2, our findings suggest a novel mechanism by which enteric microbes could influence miRNA to promote disease. |Animals [MESH] |Argonaute Proteins/genetics/*metabolism [MESH] |Autophagy-Related Protein 5 [MESH] |Autophagy-Related Protein 7 [MESH] |Autophagy/*genetics [MESH] |Bacterial Toxins/*metabolism [MESH] |Carrier Proteins [MESH] |Cell Line [MESH] |Crohn Disease/genetics/metabolism/microbiology [MESH] |Epithelial Cells/metabolism [MESH] |Fibroblasts/metabolism [MESH] |Humans [MESH] |Intestinal Mucosa/metabolism [MESH] |Mice [MESH] |Mice, Knockout [MESH] |MicroRNAs/genetics/*metabolism [MESH] |Microtubule-Associated Proteins/deficiency [MESH] |Monocytes/metabolism [MESH] |RNA-Induced Silencing Complex/metabolism [MESH]Microbial Disruption of Autophagy Alters Expression of the RISC Compon(epmc).pdf DeepDyve Pubget Overpricing