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Adenosine-to-inosine RNA editing contributes to type I interferon responses in systemic sclerosis

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Adenosine-to-inosine RNA editing contributes to type I interferon responses in systemic sclerosis. / Vlachogiannis, Nikolaos I; Tual-Chalot, Simon; Zormpas, Eleftherios et al.
In: Journal of Autoimmunity, Vol. 125, 102755, 31.12.2021.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Vlachogiannis, NI, Tual-Chalot, S, Zormpas, E, Bonini, F, Ntouros, PA, Pappa, M, Bournia, V-K, Tektonidou, MG, Souliotis, VL, Mavragani, CP, Stamatelopoulos, K, Gatsiou, A, Sfikakis, PP & Stellos, K 2021, 'Adenosine-to-inosine RNA editing contributes to type I interferon responses in systemic sclerosis', Journal of Autoimmunity, vol. 125, 102755. https://doi.org/10.1016/j.jaut.2021.102755

APA

Vlachogiannis, N. I., Tual-Chalot, S., Zormpas, E., Bonini, F., Ntouros, P. A., Pappa, M., Bournia, V.-K., Tektonidou, M. G., Souliotis, V. L., Mavragani, C. P., Stamatelopoulos, K., Gatsiou, A., Sfikakis, P. P., & Stellos, K. (2021). Adenosine-to-inosine RNA editing contributes to type I interferon responses in systemic sclerosis. Journal of Autoimmunity, 125, Article 102755. https://doi.org/10.1016/j.jaut.2021.102755

Vancouver

Vlachogiannis NI, Tual-Chalot S, Zormpas E, Bonini F, Ntouros PA, Pappa M et al. Adenosine-to-inosine RNA editing contributes to type I interferon responses in systemic sclerosis. Journal of Autoimmunity. 2021 Dec 31;125:102755. Epub 2021 Dec 10. doi: 10.1016/j.jaut.2021.102755

Author

Vlachogiannis, Nikolaos I ; Tual-Chalot, Simon ; Zormpas, Eleftherios et al. / Adenosine-to-inosine RNA editing contributes to type I interferon responses in systemic sclerosis. In: Journal of Autoimmunity. 2021 ; Vol. 125.

Bibtex

@article{c44c108649174d82adc063b6b47db380,
title = "Adenosine-to-inosine RNA editing contributes to type I interferon responses in systemic sclerosis",
abstract = "OBJECTIVE: Adenosine deaminase acting on RNA-1 (ADAR1) enzyme is a type I interferon (IFN)-stimulated gene (ISG) catalyzing the deamination of adenosine-to-inosine, a process called A-to-I RNA editing. A-to-I RNA editing takes place mainly in Alu elements comprising a primate-specific level of post-transcriptional gene regulation. Whether RNA editing is involved in type I IFN responses in systemic sclerosis (SSc) patients remains unknown.METHODS: ISG expression was quantified in skin biopsies and peripheral blood mononuclear cells derived from SSc patients and healthy subjects. A-to-I RNA editing was examined in the ADAR1-target cathepsin S (CTSS) by an RNA editing assay. The effect of ADAR1 on interferon-α/β-induced CTSS expression was assessed in human endothelial cells in vitro.RESULTS: Increased expression levels of the RNA editor ADAR1, and specifically the long ADAR1p150 isoform, and its target CTSS are strongly associated with type I IFN signature in skin biopsies and peripheral blood derived from SSc patients. Notably, IFN-α/β-treated human endothelial cells show 8-10-fold increased ADAR1p150 and 23-35-fold increased CTSS expression, while silencing of ADAR1 reduces CTSS expression by 60-70%. In SSc patients, increased RNA editing rate of individual adenosines located in CTSS 3' UTR Alu elements is associated with higher CTSS expression (r = 0.36-0.6, P < 0.05 for all). Similar findings were obtained in subjects with activated type I IFN responses including SLE patients or healthy subjects after influenza vaccination.CONCLUSION: ADAR1p150-mediated A-to-I RNA editing is critically involved in type I IFN responses highlighting the importance of post-transcriptional regulation of proinflammatory gene expression in systemic autoimmunity, including SSc.",
keywords = "Adenosine/genetics, Adenosine Deaminase/genetics, Animals, Endothelial Cells/metabolism, Humans, Inosine/genetics, Interferon Type I/metabolism, Leukocytes, Mononuclear/metabolism, RNA, RNA Editing, RNA-Binding Proteins/genetics, Scleroderma, Systemic/genetics",
author = "Vlachogiannis, {Nikolaos I} and Simon Tual-Chalot and Eleftherios Zormpas and Francesca Bonini and Ntouros, {Panagiotis A} and Maria Pappa and Vasiliki-Kalliopi Bournia and Tektonidou, {Maria G} and Souliotis, {Vassilis L} and Mavragani, {Clio P} and Kimon Stamatelopoulos and Aikaterini Gatsiou and Sfikakis, {Petros P} and Konstantinos Stellos",
note = "Copyright {\textcopyright} 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.",
year = "2021",
month = dec,
day = "31",
doi = "10.1016/j.jaut.2021.102755",
language = "English",
volume = "125",
journal = "Journal of Autoimmunity",
issn = "0896-8411",
publisher = "Academic Press",

}

RIS

TY - JOUR

T1 - Adenosine-to-inosine RNA editing contributes to type I interferon responses in systemic sclerosis

AU - Vlachogiannis, Nikolaos I

AU - Tual-Chalot, Simon

AU - Zormpas, Eleftherios

AU - Bonini, Francesca

AU - Ntouros, Panagiotis A

AU - Pappa, Maria

AU - Bournia, Vasiliki-Kalliopi

AU - Tektonidou, Maria G

AU - Souliotis, Vassilis L

AU - Mavragani, Clio P

AU - Stamatelopoulos, Kimon

AU - Gatsiou, Aikaterini

AU - Sfikakis, Petros P

AU - Stellos, Konstantinos

N1 - Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.

PY - 2021/12/31

Y1 - 2021/12/31

N2 - OBJECTIVE: Adenosine deaminase acting on RNA-1 (ADAR1) enzyme is a type I interferon (IFN)-stimulated gene (ISG) catalyzing the deamination of adenosine-to-inosine, a process called A-to-I RNA editing. A-to-I RNA editing takes place mainly in Alu elements comprising a primate-specific level of post-transcriptional gene regulation. Whether RNA editing is involved in type I IFN responses in systemic sclerosis (SSc) patients remains unknown.METHODS: ISG expression was quantified in skin biopsies and peripheral blood mononuclear cells derived from SSc patients and healthy subjects. A-to-I RNA editing was examined in the ADAR1-target cathepsin S (CTSS) by an RNA editing assay. The effect of ADAR1 on interferon-α/β-induced CTSS expression was assessed in human endothelial cells in vitro.RESULTS: Increased expression levels of the RNA editor ADAR1, and specifically the long ADAR1p150 isoform, and its target CTSS are strongly associated with type I IFN signature in skin biopsies and peripheral blood derived from SSc patients. Notably, IFN-α/β-treated human endothelial cells show 8-10-fold increased ADAR1p150 and 23-35-fold increased CTSS expression, while silencing of ADAR1 reduces CTSS expression by 60-70%. In SSc patients, increased RNA editing rate of individual adenosines located in CTSS 3' UTR Alu elements is associated with higher CTSS expression (r = 0.36-0.6, P < 0.05 for all). Similar findings were obtained in subjects with activated type I IFN responses including SLE patients or healthy subjects after influenza vaccination.CONCLUSION: ADAR1p150-mediated A-to-I RNA editing is critically involved in type I IFN responses highlighting the importance of post-transcriptional regulation of proinflammatory gene expression in systemic autoimmunity, including SSc.

AB - OBJECTIVE: Adenosine deaminase acting on RNA-1 (ADAR1) enzyme is a type I interferon (IFN)-stimulated gene (ISG) catalyzing the deamination of adenosine-to-inosine, a process called A-to-I RNA editing. A-to-I RNA editing takes place mainly in Alu elements comprising a primate-specific level of post-transcriptional gene regulation. Whether RNA editing is involved in type I IFN responses in systemic sclerosis (SSc) patients remains unknown.METHODS: ISG expression was quantified in skin biopsies and peripheral blood mononuclear cells derived from SSc patients and healthy subjects. A-to-I RNA editing was examined in the ADAR1-target cathepsin S (CTSS) by an RNA editing assay. The effect of ADAR1 on interferon-α/β-induced CTSS expression was assessed in human endothelial cells in vitro.RESULTS: Increased expression levels of the RNA editor ADAR1, and specifically the long ADAR1p150 isoform, and its target CTSS are strongly associated with type I IFN signature in skin biopsies and peripheral blood derived from SSc patients. Notably, IFN-α/β-treated human endothelial cells show 8-10-fold increased ADAR1p150 and 23-35-fold increased CTSS expression, while silencing of ADAR1 reduces CTSS expression by 60-70%. In SSc patients, increased RNA editing rate of individual adenosines located in CTSS 3' UTR Alu elements is associated with higher CTSS expression (r = 0.36-0.6, P < 0.05 for all). Similar findings were obtained in subjects with activated type I IFN responses including SLE patients or healthy subjects after influenza vaccination.CONCLUSION: ADAR1p150-mediated A-to-I RNA editing is critically involved in type I IFN responses highlighting the importance of post-transcriptional regulation of proinflammatory gene expression in systemic autoimmunity, including SSc.

KW - Adenosine/genetics

KW - Adenosine Deaminase/genetics

KW - Animals

KW - Endothelial Cells/metabolism

KW - Humans

KW - Inosine/genetics

KW - Interferon Type I/metabolism

KW - Leukocytes, Mononuclear/metabolism

KW - RNA

KW - RNA Editing

KW - RNA-Binding Proteins/genetics

KW - Scleroderma, Systemic/genetics

U2 - 10.1016/j.jaut.2021.102755

DO - 10.1016/j.jaut.2021.102755

M3 - Journal article

C2 - 34857436

VL - 125

JO - Journal of Autoimmunity

JF - Journal of Autoimmunity

SN - 0896-8411

M1 - 102755

ER -