The DOI matches its Crossref record; 66 of the 66 references it cites were found in a registry or an index.
A role for NF-κB–dependent gene transactivation in sunburn
Open accessAbstract
Exposure of skin to ultraviolet (UV) radiation is known to induce NF-kappaB activation, but the functional role for this pathway in UV-induced cutaneous inflammation remains uncertain. In this study, we examined whether experimentally induced sunburn reactions in mice could be prevented by blocking UV-induced, NF-kappaB-dependent gene transactivation with oligodeoxynucleotides (ODNs) containing the NF-kappaB cis element (NF-kappaB decoy ODNs). UV-induced secretion of IL-1, IL-6, TNF-alpha, and VEGF by skin-derived cell lines was inhibited by the decoy ODNs, but not by the scrambled control ODNs. Systemic or local injection of NF-kappaB decoy ODNs also inhibited cutaneous swelling responses to UV irradiation. Moreover, local UV-induced inflammatory changes (swelling, leukocyte infiltration, epidermal hyperplasia, and accumulation of proinflammatory cytokines) were all inhibited specifically by topically applied decoy ODNs. Importantly, these ODNs had no effect on alternative types of cutaneous inflammation caused by irritant or allergic chemicals. These results indicate that sunburn reactions culminate from inflammatory events that are triggered by UV-activated transcription of NF-kappaB target genes, rather than from nonspecific changes associated with tissue damage.
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“However, it is likely that the photoprotective activity of vitamin D compounds includes a reduction in skin inflammation, which plays a crucial role in sunburn formation [104].”
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Metadata
- Authors
- Abeyama, K., Eng, W., Jester, J. V., Vink, A. A., Edelbaum, D., Cockerell, C. J., Bergstresser, P. R., & Takashima, A.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Netherlands Organisation for Applied Scientific Research (NL)
- Corresponding author
- Takashima, Akira
- Venue
- Journal of Clinical Investigation
- Published
- 2000-06-15
- Volume
- 105
- Issue
- 12
- Pages
- 1751-1759
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC378515
- OpenAlex
- W2136200385
- Cited by
- 160
- References
- 66
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 4 · 2023: 3 · 2022: 3 · 2021: 9 · 2020: 1 · 2019: 7 · 2018: 7 · 2017: 1 · 2016: 11 · 2015: 3 · 2014: 3 · 2013: 5 · 2012: 3
- FWCI
- 4.75
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01 AR 35068, R01-AR40042, R01-AR43777, R01AR040042, R01AR043777, R01AR035068)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- NF-κB, sunburn, ultraviolet radiation, skin inflammation, decoy oligonucleotides, gene transactivation, inflammatory cytokines, interleukin-1, interleukin-6, TNF-α, vascular endothelial growth factor, epidermal hyperplasia, leukocyte infiltration, topical gene therapy
- MeSH terms
- Animals, Base Sequence, Cell Line, Edema, Female, Gene Expression Regulation, Hyperplasia, Langerhans Cells, Mice, Inbred A, Mice, Inbred BALB C, Oligodeoxyribonucleotides, Skin, Sunburn, Ultraviolet Rays, Transcriptional Activation, Keratinocytes, NF-kappa B, Mice
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