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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Adolescent, Adult, Aged, Animals, Basic Helix-Loop-Helix Transcription Factors, Biomarkers, Caco-2 Cells, Colitis, Colon, Crohn Disease, Cytokines, Down-Regulation, Female, HT29 Cells, Humans, Intestinal Mucosa, Male, Mice, Mice, Inbred BALB C, MicroRNAs, Middle Aged, Real-Time Polymerase Chain Reaction, Receptors, Aryl Hydrocarbon, Trinitrobenzenesulfonic Acid, Up-Regulation, Young Adult.
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Does microRNA-124 promote Intestinal Inflammation by Targeting Aryl Hydrocarbon Receptor in Crohn 's Disease? Context: Dysregulation of microRNAs (miRNAs) is associated with a variety of diseases, including Crohn's disease (CD), but the essential biological functions and crucial targets of miRNAs remain largely unknown. The present study investigated the aberrant colonic mucosal miRNAs in active CD patients. miRNA levels were assayed in inflamed colon of active CD patients by quantitative real-time polymerase chain reaction. The influence of differential expressed miR-124 on its putative target, the aryl hydrocarbon receptor (AHR), was investigated in CD patients, intestinal epithelial cells (IECs) and 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis mice. The role of miR-124 was further studied in experimental colitis mice by intracolonic administration of miR-124 inhibitors or precursors. We found an inverse correlation between miR-124 and AHR protein levels in colon tissues and IECs of active CD patients. Further results demonstrated that miR-124 suppressed AHR expression by directly targeting the AHR 3'-untranslated region (3'-UTR) in Caco-2 cells and HT-29 cells. MiR-124 mediated the inflammatory response in lipopolysaccharide-stimulated cells through retroregulation of AHR in vitro. Downregulation or upregulation of miR-124 in TNBS-induced colitic colon alleviated or aggravated experimental colitis, respectively.
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These findings suggest that miR-124 induces intestinal inflammation by inhibiting AHR to modulate pro-inflammatory cytokine production and thereby promotes the pathogenesis of CD. Final Decision: yes