LncRNA ARGI Contributes to Virus‐Induced Pancreatic β Cell Inflammation Through Transcriptional Activation of IFN‐Stimulated Genes

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 disrup...

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Veröffentlicht in:Advanced science Jg. 10; H. 25; S. e2300063 - n/a
Hauptverfasser: González‐Moro, Itziar, Garcia‐Etxebarria, Koldo, Mendoza, Luis Manuel, Fernández‐Jiménez, Nora, Mentxaka, Jon, Olazagoitia‐Garmendia, Ane, Arroyo, María Nicol, Sawatani, Toshiaki, Moreno‐Castro, Cristina, Vinci, Chiara, Op de Beek, Anne, Cnop, Miriam, Igoillo‐Esteve, Mariana, Santin, Izortze
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Germany John Wiley & Sons, Inc 01.09.2023
John Wiley and Sons Inc
Wiley
Schlagworte:
Cells
Diabetes Mellitus, Type 1
Disease
Gene expression
Genomes
Humans
Infections
Inflammation
Inflammation - metabolism
Insulin
Insulin-Secreting Cells
long non‐coding RNAs
pancreatic β cells
Pathogenesis
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Signal transduction
single nucleotide polymorphism
Student's t-test
Transcriptional Activation - genetics
type 1 diabetes
Viral infections
type 1 diabetes
viral infections
long non-coding RNAs
single nucleotide polymorphism
pancreatic β cells
ISSN:2198-3844, 2198-3844
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Abstract 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. Long non‐coding RNAs (lncRNAs) are emerging as regulators for several molecular processes that are important for human diseases. Herein, the function of a type 1 diabetes (T1D)‐associated lncRNA named ARGI is described. ARGI modulates the transcription of virus‐induced IFNβ and interfer on stimulated genes (ISGs) in pancreatic β cells in an allele‐specific manner.
AbstractList 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. Long non‐coding RNAs (lncRNAs) are emerging as regulators for several molecular processes that are important for human diseases. Herein, the function of a type 1 diabetes (T1D)‐associated lncRNA named ARGI is described. ARGI modulates the transcription of virus‐induced IFNβ and interfer on stimulated genes (ISGs) in pancreatic β cells in an allele‐specific manner.
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.
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.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.
Abstract 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.
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. Long non‐coding RNAs (lncRNAs) are emerging as regulators for several molecular processes that are important for human diseases. Herein, the function of a type 1 diabetes (T1D)‐associated lncRNA named ARGI is described. ARGI modulates the transcription of virus‐induced IFNβ and interfer on stimulated genes (ISGs) in pancreatic β cells in an allele‐specific manner.
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 IFN β 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.
Author Olazagoitia‐Garmendia, Ane
Arroyo, María Nicol
Moreno‐Castro, Cristina
Op de Beek, Anne
González‐Moro, Itziar
Mentxaka, Jon
Cnop, Miriam
Igoillo‐Esteve, Mariana
Fernández‐Jiménez, Nora
Sawatani, Toshiaki
Vinci, Chiara
Garcia‐Etxebarria, Koldo
Mendoza, Luis Manuel
Santin, Izortze
AuthorAffiliation 3 Biodonostia Health Research Institute Gastrointestinal Genetics Group San Sebastián 20014 Spain
5 Department of Genetics Physical Anthropology and Animal Physiology University of the Basque Country Leioa 48940 Spain
8 Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM) Instituto de Salud Carlos III Madrid 28029 Spain
4 Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd) Barcelona 08036 Spain
7 Division of Endocrinology Erasmus Hospital Université Libre de Bruxelles Brussels 1070 Belgium
1 Department of Biochemistry and Molecular Biology University of the Basque Country Leioa 48940 Spain
6 ULB Center for Diabetes Research Université Libre de Bruxelles Brussels 1070 Belgium
2 Biocruces Bizkaia Health Research Institute Barakaldo 48903 Spain
AuthorAffiliation_xml – name: 6 ULB Center for Diabetes Research Université Libre de Bruxelles Brussels 1070 Belgium
– name: 4 Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd) Barcelona 08036 Spain
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/37382191$$D View this record in MEDLINE/PubMed
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Issue 25
Keywords type 1 diabetes
viral infections
long non-coding RNAs
single nucleotide polymorphism
pancreatic β cells
Language English
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2023 The Authors. Advanced Science published by Wiley-VCH GmbH.
This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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Snippet Type 1 diabetes (T1D) is a complex autoimmune disease that develops in genetically susceptible individuals. Most T1D‐associated single nucleotide polymorphisms...
Type 1 diabetes (T1D) is a complex autoimmune disease that develops in genetically susceptible individuals. Most T1D-associated single nucleotide polymorphisms...
Abstract Type 1 diabetes (T1D) is a complex autoimmune disease that develops in genetically susceptible individuals. Most T1D‐associated single nucleotide...
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StartPage e2300063
SubjectTerms Cells
Diabetes Mellitus, Type 1
Disease
Gene expression
Genomes
Humans
Infections
Inflammation
Inflammation - metabolism
Insulin
Insulin-Secreting Cells
long non‐coding RNAs
pancreatic β cells
Pathogenesis
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Signal transduction
single nucleotide polymorphism
Student's t-test
Transcriptional Activation - genetics
type 1 diabetes
Viral infections
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Title LncRNA ARGI Contributes to Virus‐Induced Pancreatic β Cell Inflammation Through Transcriptional Activation of IFN‐Stimulated Genes
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fadvs.202300063
https://www.ncbi.nlm.nih.gov/pubmed/37382191
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Volume 10
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