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Characterization of LncRNA BC012900 among long non-coding RNAs differentially expressed in ulcerative colitis

ABSTRACT: In this report, we provide a comprehensive assessment of the expression of ~17000 lncRNAs on 60 colonic samplesin colon tissues from patients with IBD, irritable bowel syndrome, infectious colitis and healthy controls. We also explored the possibility of using cRNAs as biomarkers distinguish active UC from normal. To investigate the mechanism offunctional role these IBD-associated lncRNAs in the development of IBD, we then focused on a ncRNA highlyexpressed in the UC-associated lncRNAactive UC, BC012900. We , to characterized its cellular localization, expression regulation and biological function. We . We found that BC012900 and its adjacent gene, dual specificity phosphatase 4 (DUSP4) are functionally distinct, with BC012900 modulating. Overexpression of BC012900 resulted in usceptibility to apoptosis. Our study provides the first evidence that lncRNAs may play potential roles in development and persistence of active UC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE72221 | GEO | 2016/01/28

SECONDARY ACCESSION(S): PRJNA293411

REPOSITORIES: GEO

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Project description:Background & Aims: Inflammatory bowel diseases (IBD) are clinically manifested as ulcerative colitis (UC) and Crohn’s Disease (CD). Novel high throughput technologies revealed new categories of genes, including the long non-coding RNAs (lncRNAs), which have been involved in the pathogenesis of different human diseases; however the role and function of lncRNAs in the UC pathogenesis has not been evaluated. Methods: The gene expression patterns for both non-coding (lncRNAs) and coding (mRNA) transcripts were profiled in UC (n=8) and control (n=7) patients by ArrayStar assays. The differentially expressed genes were used to develop lncRNA signatures in UC samples. Ingenuity Software Analysis (IPA) program was used to identify the up-stream regulators of IFNG-AS1. Jurkat T cells were activated by PMA/ionomycin and IFNG and TNF protein levels were assessed by ELISA assay. Two anti-sense molecules were designed and used to block IFNG-AS1 expression levels. Colonic tissues from TNBS-treated and IL10-/- mice were used to extract RNA and examine INFG-AS1 expression by real-time PCR. Results: A unique set of lncRNAs was found to be differentially expressed between UC (n=15) and control samples (n=16). Of these, IFNG-AS1 was among the highest statistically significant lncRNAs (fold change: 5.27, p-value: 7.07E-06). Bioinformatic analyses showed that IFNG-AS1 was associated with the IBD susceptibility loci SNP rs7134599 and its genomic location is adjacent to the inflammatory cytokine, interferon-gamma (IFNG). Using the TNBS and IL10-/- mouse models of colitis, we found increased colonic expression of this lncRNA during active colitis. Utilizing the Jurkat T cell model system, we explored the mechanisms of action and found that IFNG-AS1 can positively regulate IFNG expression. Conclusions: Novel lncRNA signatures were identified to differentiate UC patients with active disease, in remission and control subjects. A subset of these lncRNAs was found to be associated with the clinically validated IBD susceptibility loci. IFNG-AS1 was one of these differentially expressed lncRNAs in UC patients and was found to regulate the key inflammatory cytokine, IFNG, in CD4 T cells. Taken together, our study revealed novel lncRNA signatures deregulated in ulcerative colitis and identified IFNG-AS1 as a novel regulator of IFNG inflammatory responses, suggesting the potential importance of non-coding RNA mechanisms on regulation of IBD-related inflammatory responses.

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Characterization of LncRNA BC012900 among long non-coding RNAs differentially expressed in ulcerative colitis

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