LncRNA ARGI Contributes to Virus-Induced Pancreatic β Cell Inflammation Through Transcriptional Activation of IFN-Stimulated Genes.
long non-coding RNAs
pancreatic β cells
single nucleotide polymorphism
type 1 diabetes
viral infections
Journal
Advanced science (Weinheim, Baden-Wurttemberg, Germany)
ISSN: 2198-3844
Titre abrégé: Adv Sci (Weinh)
Pays: Germany
ID NLM: 101664569
Informations de publication
Date de publication:
09 2023
09 2023
Historique:
revised:
30
05
2023
received:
04
01
2023
medline:
6
9
2023
pubmed:
29
6
2023
entrez:
29
6
2023
Statut:
ppublish
Résumé
Type 1 diabetes (T1D) is a complex autoimmune disease that develops in genetically susceptible individuals. Most T1D-associated single nucleotide polymorphisms (SNPs) are located in non-coding regions of the human genome. Interestingly, SNPs in long non-coding RNAs (lncRNAs) may result in the disruption of their secondary structure, affecting their function, and in turn, the expression of potentially pathogenic pathways. In the present work, the function of a virus-induced T1D-associated lncRNA named ARGI (Antiviral Response Gene Inducer) is characterized. Upon a viral insult, ARGI is upregulated in the nuclei of pancreatic β cells and binds to CTCF to interact with the promoter and enhancer regions of IFNβ and interferon-stimulated genes, promoting their transcriptional activation in an allele-specific manner. The presence of the T1D risk allele in ARGI induces a change in its secondary structure. Interestingly, the T1D risk genotype induces hyperactivation of type I IFN response in pancreatic β cells, an expression signature that is present in the pancreas of T1D patients. These data shed light on the molecular mechanisms by which T1D-related SNPs in lncRNAs influence pathogenesis at the pancreatic β cell level and opens the door for the development of therapeutic strategies based on lncRNA modulation to delay or avoid pancreatic β cell inflammation in T1D.
Identifiants
pubmed: 37382191
doi: 10.1002/advs.202300063
pmc: PMC10477904
doi:
Substances chimiques
RNA, Long Noncoding
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e2300063Subventions
Organisme : European Foundation for the Study of Diabetes
ID : EFSD/JDRF/LillyProgrammeonType1DiabetesResearch
Organisme : Ministry of Science and Innovation, MCIN/AEI/10.13039/501100011033
ID : PID2019-104475GA-I00
Informations de copyright
© 2023 The Authors. Advanced Science published by Wiley-VCH GmbH.
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