Nox1-Based NADPH Oxidase Is the Major Source of UVA-Induced Reactive Oxygen Species in Human Keratinocytes
Open accessAbstract
UVA radiation is a major environmental stress on skin, causing acute and chronic photodamage. These responses are mediated by reactive oxygen species (ROS), although the cellular source of these ROS is unknown. We tested the hypotheses that UVA-induced activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is required for ROS generation in human keratinocytes (HK) and that these ROS initiate rapid prostaglandin E2 (PGE2) synthesis. Treatment of HK with a non-toxic dose of UVA rapidly increased NADPH oxidase activity and intracellular ROS, which were partially blocked by an inhibitor of NADPH oxidase and by a mitochondria-selective antioxidant. Depleting the Nox1 isoform of the catalytic subunit of NADPH oxidase using small interfering RNA (siRNA) blocked the UVA-induced ROS increase, indicating that ROS produced by mitochondria or other sources are downstream from Nox1. Nox1 siRNA also blocked UVA-initiated PGE2 synthesis. The mechanism for activation of Nox1 is mediated by an increase in intracellular calcium. Ceramide, which has been proposed to mediate responses to UVA in HK, also activated NADPH oxidase. These results indicate that UVA activates Nox1-based NADPH oxidase to produce ROS that stimulate PGE2 synthesis, and that Nox1 may be an appropriate target for agents designed to block UVA-induced skin injury.
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The UVB dark CPD process depends on melanin and is distinct from delayed CPD reported in other cell types after UVC or UVB.
“The UVB process was also dependent on melanin and thus it differs from the delayed production of CPD that has been reported occasionally in other cell types after UVC or UVB exposure (16-18).”
From Chemiexcitation of melanin derivatives induces DNA photoproducts long after UV exposure (2015) · cites this paper as [18]
The UVA irradiation and NADPH oxidase sections describe reactive oxygen species in UVA-exposed keratinocytes, not UVB-induced dark CPDs. Searches for melanin, CPDs, and delayed CPD production after UVB or UVC found no passage addressing the claim in our copy. (LLM, conf=0.75)
Experimental — accuracy not yet measuredThe melanin requirement for nuclear nitration suggests that the nitric oxide requirement in melanocytes differs from that in cultured keratinocytes.
“The melanin requirement suggests that the NO• requirement in melanocytes is distinct from that observed in cultured keratinocytes (18).”
From Chemiexcitation of melanin derivatives induces DNA photoproducts long after UV exposure (2015) · cites this paper as [18]
The Discussion (page unavailable) describes UVA-induced reactive oxygen species in keratinocytes as arising primarily through Nox1-based NADPH oxidase. It does not address a nitric oxide requirement in keratinocytes or compare one with melanocytes; searches for nitric oxide, NO synthase, and nitration found no passage supporting that comparison. (LLM, conf=0.75)
Experimental — accuracy not yet measuredA growing body of evidence suggests that mitochondria, ferritin and NADPH oxidase (Nox-1) participate in UVA-induced DNA damage.
“Furthermore, a growing body of evidence has suggested that mitochondria, ferritin and NADPH oxidase (Nox-1) participate in the UVA-induced DNA damage [86,87].”
From Sunlight damage to cellular DNA: focus on oxidatively generated lesions (2017) · cites this paper as [86]
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- Authors
- Valencia, A., & Kochevar, I. E.
- Affiliations
- Harvard University (US)
- Corresponding author
- Kochevar, Irene E.
- ORCID
- Kochevar, Irene E.
- Venue
- Journal of Investigative Dermatology
- Publisher
- Elsevier BV
- Published
- 2008-01
- Volume
- 128
- Issue
- 1
- Pages
- 214-222
- ISSN
- 0022-202X (ISSN-L)
- OpenAlex
- W2066589243
- Cited by
- 194
- References
- 54
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 5 · 2023: 5 · 2022: 10 · 2021: 16 · 2020: 7 · 2019: 11 · 2018: 13 · 2017: 14 · 2016: 8 · 2015: 12 · 2014: 17 · 2013: 9 · 2012: 8
- FWCI
- 12.39
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Investigative Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of General Medical Sciences (GM-30955)
- Topics
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Keywords
- NOX1, NADPH oxidase, UVA, reactive oxygen species, human keratinocytes, prostaglandin E2 synthesis, photodamage, intracellular calcium, ceramide, mitochondria, skin damage
- MeSH terms
- NADPH Oxidase 1, Calcium, Cells, Cultured, Ceramides, Humans, Onium Compounds, Ultraviolet Rays, Dinoprostone, Keratinocytes, Reactive Oxygen Species, NADPH Oxidases, RNA, Small Interfering
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