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Numerous genome-wide association studies demonstrate that a variant in the autophagy-dependent gene ATG16L1 is associated with Crohn's Disease (CD). miRNA regulation has been shown to contribute to the pathogenesis of many inflammatory diseases including inflammatory bowel disease. miRNA bind to the complementary 3' untranslated region (UTR) of the target mRNA to repress their translation and promote their degradation. Here we investigated the functional effect of miR-142-3p on ATG16L1 and autophagy. HeLa and HCT116 cells were transfected with either a miR-142-3p mimic or antagonist and qPCR for ATG16L1 and western blotting was performed. In comparison to control cells, a decrease in ATG16L1 transcripts was detected in cells transfected with the miR-142-3p mimic. A reduction in ATG16L1 and LC3-II protein level was also seen in immunoblots. Taken together, these results indicate that miR-142- 3p can directly regulate ATG16L1 and repress autophagy, implicating miRNA regulation in the pathogenesis of CD.