A long noncoding RNA associated with susceptibility to celiac disease

Recent studies have implicated long noncoding RNAs (IncRNAs) as regulators of many important biological processes. Here we report on the identification and characterization of a IncRNA, Inc13, that harbors a celiac disease–associated haplotype block and represses expression of certain inflammatory g...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 2016-04, Vol.352 (6281), p.91-95
Main Authors: Castellanos-Rubio, Ainara, Fernandez-Jimenez, Nora, Kratchmarov, Radomir, Luo, Xiaobing, Bhagat, Govind, Green, Peter H. R., Schneider, Robert, Kiledjian, Megerditch, Bilbao, Jose Ramon, Ghosh, Sankar
Format: Article
Language:English
Subjects:
Animals
Autoimmune diseases
Base Sequence
Celiac disease
Celiac Disease - genetics
Celiac Disease - pathology
Down-Regulation
Gene expression
Gene Expression Regulation
Genetic Predisposition to Disease
Haplotypes
Heterogeneous-Nuclear Ribonucleoproteins - genetics
Humans
Inflammation
Inflammation - genetics
Mice
Molecular Sequence Data
Pathogenesis
Polymorphism, Single Nucleotide
Ribonucleic acid
RNA
RNA, Long Noncoding - genetics
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Summary:Recent studies have implicated long noncoding RNAs (IncRNAs) as regulators of many important biological processes. Here we report on the identification and characterization of a IncRNA, Inc13, that harbors a celiac disease–associated haplotype block and represses expression of certain inflammatory genes under homeostatic conditions. Lnc13 regulates gene expression by binding to hnRNPD, a member of a family of ubiquitously expressed heterogeneous nuclear ribonucleoproteins (hnRNPs). Upon stimulation, Inc13 levels are reduced, thereby allowing increased expression of the repressed genes. Lnc13 levels are significantly decreased in small intestinal biopsy samples from patients with celiac disease, which suggests that down-regulation of Inc13 may contribute to the inflammation seen in this disease. Furthermore, the Inc13 disease-associated variant binds hnRNPD less efficiently than its wild-type counterpart, thus helping to explain how these single-nucleotide polymorphisms contribute to celiac disease.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.aad0467