Substrate-specific binding of 8-oxoguanine DNA glycosylase 1 (OGG1) reprograms mucosal adaptations to chronic airway injury.

NFκB ROS SMADs epigenetics inflammation remodeling

Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2023
Historique:
received: 14 03 2023
accepted: 24 07 2023
medline: 25 8 2023
pubmed: 24 8 2023
entrez: 24 8 2023
Statut: epublish

Résumé

Recent advances have uncovered the non-random distribution of 7, 8-dihydro-8-oxoguanine (8-oxoGua) induced by reactive oxygen species, which is believed to have epigenetic effects. Its cognate repair protein, 8-oxoguanine DNA glycosylase 1 (OGG1), reads oxidative substrates and participates in transcriptional initiation. When redox signaling is activated in small airway epithelial cells, the DNA repair function of OGG1 is repurposed to transmit acute inflammatory signals accompanied by cell state transitions and modification of the extracellular matrix. Epithelial-mesenchymal and epithelial-immune interactions act cooperatively to establish a local niche that instructs the mucosal immune landscape. If the transitional cell state governed by OGG1 remains responsive to inflammatory mediators instead of differentiation, the collateral damage provides positive feedback to inflammation, ascribing inflammatory remodeling to one of the drivers in chronic pathologies. In this review, we discuss the substrate-specific read through OGG1 has evolved in regulating the innate immune response, controlling adaptations of the airway to environmental and inflammatory injury, with a focus on the reader function of OGG1 in initiation and progression of epithelial to mesenchymal transitions in chronic pulmonary disease.

Identifiants

pubmed: 37614238
doi: 10.3389/fimmu.2023.1186369
pmc: PMC10442650
doi:

Substances chimiques

8-hydroxyguanine 5614-64-2
Guanine 5Z93L87A1R
DNA Glycosylases EC 3.2.2.-

Types de publication

Journal Article Review Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1186369

Informations de copyright

Copyright © 2023 Pan, Vlahopoulos, Tanner, Bergwik, Bacsi, Radak, Egesten, Ba, Brasier and Boldogh.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Lang Pan (L)

Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, United States.

Spiros Vlahopoulos (S)

Horemeio Research Laboratory, First Department of Pediatrics, National and Kapodistrian University of Athens, Athens, Greece.

Lloyd Tanner (L)

Respiratory Medicine, Allergology & Palliative Medicine, Department of Clinical Sciences Lund, Lund University and Skåne University Hospital, Lund, Sweden.

Jesper Bergwik (J)

Respiratory Medicine, Allergology & Palliative Medicine, Department of Clinical Sciences Lund, Lund University and Skåne University Hospital, Lund, Sweden.

Attila Bacsi (A)

Department of Immunology, Faculty of Medicine, University of Debrecen, Hungary, Debrecen, Hungary.

Zsolt Radak (Z)

Research Institute of Sport Science, University of Physical Education, Budapest, Hungary.

Arne Egesten (A)

Respiratory Medicine, Allergology & Palliative Medicine, Department of Clinical Sciences Lund, Lund University and Skåne University Hospital, Lund, Sweden.

Xueqing Ba (X)

Key Laboratory of Molecular Epigenetics of Ministry of Education, School of Life Science, Northeast Normal University, Changchun, Jilin, China.

Allan R Brasier (AR)

Department of Medicine, University of Wisconsin-Madison School of Medicine and Public Health (SMPH), Madison, WI, United States.

Istvan Boldogh (I)

Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, United States.

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Classifications MeSH