NF-κB pathway related long non-coding RNAs in inflammatory bowel disease

Abstract

Abstract Background: Inflammatory bowel disease (IBD) is a complex disease classified into two types, ulcerative colitis (UC) and Crohn’s disease (CD), and it results from the interaction between genetic and environmental factors influencing immune responses. However, the etiology of the IBD has not yet been fully understood. The nuclear factor kappa beta (NF-κB) pathway is one of the major regulators of inflammatory responses associated with the pathogenesis of IBD. The up-regulation in NF-κB expression in mucosal macrophages and monocytes induces increased production of pro-inflammatory cytokines. Several recent studies have indicated abnormal function and expression levels of non-coding RNAs, including lncRNAs, in the pathogenesis of IBD. Various lncRNAs, involved in immune responses were suggested to associate with IBD pathogenesis and maintenance of intestinal mucosa function via the interaction network between miRNAs, transcription factors, and mRNAs. Method: In this study, we aimed to predict regulatory lncRNAs for the NF-κB pathway with bioinformatics studies and validate the expression of 4 predicted lncRNAs (NRAV, HULC, RAD51-AS1, and SBF2-AS1) in blood and tissue samples of UC patients. Results: The qPCR results indicated that NRAV and HULC are upregulated in UC colonic samples, and RAD51-AS1 and SBF2-AS1 are upregulated in blood samples of UC patients compared to controls. Conclusion: This study indicated that bioinformatics studies could successfully predict disease-related lncRNAs and studied lncRNAs such as HULC, NRAV, RAD51-AS1 and SBF2-AS1 may have and important role in controlling inflammation in IBD.