Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 134, Issue 4, Pages 1083-1090Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/jid.2013.479
Keywords
-
Categories
Funding
- CDMRP grant from the US Department of Defense [CA093588]
- MGH Millennium Melanoma Fund
- National Institutes of Health [K24 CA149202]
- CDMRP [CA093588, 545607] Funding Source: Federal RePORTER
Ask authors/readers for more resources
Long-wave UVA is the major component of terrestrial UV radiation and is also the predominant constituent of indoor sunlamps, both of which have been shown to increase cutaneous melanoma risk. Using a two-chamber model, we show that UVA-exposed target cells induce intercellular oxidative signaling to non-irradiated bystander cells. This UVA-mediated bystander stress is observed between all three cutaneous cell types (i.e., keratinocytes, melanocytes, and fibroblasts). Significantly, melanocytes appear to be more resistant to direct UVA effects compared with keratinocytes and fibroblasts, although melanocytes are also more susceptible to bystander oxidative signaling. The extensive intercellular flux of oxidative species has not been previously appreciated and could possibly contribute to the observed cancer risk associated with prolonged UVA exposure.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available