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Genome Med. 2015 May 13;7(1):39. doi: 10.1186/s13073-015-0162-2. eCollection 2015.

Transcriptomic landscape of lncRNAs in inflammatory bowel disease.

Author information

1
Center for non-coding RNA in Technology and Health, University of Copenhagen, Frederiksberg, 1870 Denmark ; Department of Pediatrics E, Copenhagen Diabetes Research Center (CPH-DIRECT), Herlev University Hospital, Herlev, 2730 Denmark ; Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, 2200 Denmark.
2
Center for non-coding RNA in Technology and Health, University of Copenhagen, Frederiksberg, 1870 Denmark ; Department of Obesity Biology, Novo Nordisk, Måløv, 2760 Denmark.
3
Center for non-coding RNA in Technology and Health, University of Copenhagen, Frederiksberg, 1870 Denmark ; Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, 2200 Denmark.
4
Center for non-coding RNA in Technology and Health, University of Copenhagen, Frederiksberg, 1870 Denmark ; Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, 2200 Denmark ; The Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, Copenhagen, 2200 Denmark.
5
Department of Molecular Genetics, Novo Nordisk, Måløv, 2760 Denmark.
6
Department of Surgery, North Zealand Hospital, Hillerød, 3400 Denmark.

Abstract

BACKGROUND:

Inflammatory bowel disease (IBD) is a complex multi-factorial inflammatory disease with Crohn's disease (CD) and ulcerative colitis (UC) being the two most common forms. A number of transcriptional profiling studies have provided compelling evidence that describe the role of protein-coding genes and microRNAs in modulating the immune responses in IBD.

METHODS:

In the present study, we performed a genome-wide transcriptome profiling of lncRNAs and protein-coding genes in 96 colon pinch biopsies (inflamed and non-inflamed) extracted from multiple colonic locations from 45 patients (CD = 13, UC = 20, controls = 12) using an expression microarray platform.

RESULTS:

In our study, we identified widespread dysregulation of lncRNAs and protein-coding genes in both inflamed and non-inflamed CD and UC compared to the healthy controls. In cases of inflamed CD and UC, we identified 438 and 745 differentially expressed lncRNAs, respectively, while in cases of the non-inflamed CD and UC, we identified 12 and 19 differentially expressed lncRNAs, respectively. We also observed significant enrichment (P-value <0.001, Pearson's Chi-squared test) for 96 differentially expressed lncRNAs and 154 protein-coding genes within the IBD susceptibility loci. Furthermore, we found strong positive expression correlations for the intersecting and cis-neighboring differentially expressed IBD loci-associated lncRNA-protein-coding gene pairs. The functional annotation analysis of differentially expressed genes revealed their involvement in the immune response, pro-inflammatory cytokine activity and MHC protein complex.

CONCLUSIONS:

The lncRNA expression profiling in both inflamed and non-inflamed CD and UC successfully stratified IBD patients from the healthy controls. Taken together, the identified lncRNA transcriptional signature along with clinically relevant parameters suggest their potential as biomarkers in IBD.

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