Guanine Deaminase Stimulates Ultraviolet-Induced Keratinocyte Senescence in Seborrhoeic Keratosis via Guanine Metabolites
Open accessAbstract
DNA damage and oxidative stress play a critical role in photoageing. Seborrhoeic keratosis (SK) affects sunlight-exposed sites in aged individuals. This study examined the mechanism of photoageing in SK. The guanine deaminase gene, which is involved in purine metabolism, was upregulated with uric acid levels and p21 in SK. Guanine deaminase was detectable in keratinocytes. Repeated exposure to ultraviolet (UV) increased levels of guanine deaminase, together with DNA damage, such as γ-H2AX and cyclobutane pyrimidine dimer formation, generation of reactive oxygen species, and keratinocyte senescence, which were reversed by guanine deaminase knockdown. However, guanine deaminase overexpression and H2O2 formed γ-H2AX, but not cyclobutane pyrimidine dimer. Loss-of-function guanine deaminase mutants reduced the metabolic end-product uric acid, which was increased by exposure to exogenous xanthine. Repeated exposure to UV increased levels of uric acid. Exogenous uric acid increased cellular senescence, reactive oxygen species, and γ-H2AX, similar to guanine deaminase. Overall, guanine deaminase upregulation increased UV-induced keratinocyte senescence in SK, via uric acid mediated by reactive oxygen species followed by DNA damage.
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Keratinocyte exposure to exogenous UA triggers cellular senescence and OS through a mechanism at the basis of UV-induced damage.
“For example, keratinocyte exposure to exogenous UA triggers cellular senescence and OS through a mechanism that is at the basis of the UV-induced damage [220]”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [220]
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References 44 · Cited by 21
- Authors
- Cheong, K., & Lee, A.
- Affiliations
- Dongguk University Ilsan Hospital (KR)
- Corresponding author
- Lee, A
- ORCID
- Lee, A
- Venue
- Acta Dermato Venereologica
- Published
- 2020
- Volume
- 100
- Issue
- 8
- Pages
- adv00109-10
- ISSN
- 0001-5555 (ISSN-L)
- 1651-2057
- PMC
- PMC9128948
- OpenAlex
- W3013510533
- Cited by
- 21
- References
- 44
- Citations by year
- 2026: 3 · 2025: 1 · 2023: 6 · 2022: 5 · 2021: 5 · 2020: 1
- FWCI
- 3.10
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc
- Locations
- Acta Dermato Venereologica (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Research Foundation (2018R1A5A2023127)
- National Research Foundation of Korea (2018R1A5A2023127, NRF-2017R1A2A2A09069507, NRF-2018R1A5A 2023127)
- Ministry of Science and ICT, South Korea (NRF 2018R1A5A2023127, 2018R1A5A2023127)
- Topics
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Health Sciences › Medicine › Epidemiology › Nonmelanoma Skin Cancer Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Biochemical and Molecular Research
- Keywords
- guanine deaminase, seborrheic keratosis, keratinocyte senescence, ultraviolet radiation, photoaging, uric acid, reactive oxygen species, DNA damage, γH2AX, cyclobutane pyrimidine dimers, purine metabolism, xanthine, p21
- MeSH terms
- Adult, Aged, Cells, Cultured, DNA Damage, Female, Guanine, Guanine Deaminase, Histones, Humans, Male, Middle Aged, Pyrimidine Dimers, Ultraviolet Rays, Uric Acid, Skin Aging, Keratinocytes, Up-Regulation, Cellular Senescence, Reactive Oxygen Species, Keratosis, Seborrheic, Xanthine, Cyclin-Dependent Kinase Inhibitor p21
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