Abstract
Excessive sun exposure or high acute doses of ultraviolet (UV)-B radiation promote cutaneous inflammation and genetic mutations, both of which can ultimately contribute to skin carcinogenesis. A major mediator synthesized in the epidermis in response to UVB irradiation is the secosteroid hormone vitamin D 3, and as such, considerable attention is now turning to the many physiologic processes that it regulates. Recent studies have uncovered an immunoregulatory interaction between vitamin D 3 and dermal mast cells for optimal protection against pathogenic outcomes associated with chronic UVB irradiation of the skin. Most biological effects of vitamin D 3, such as the regulation of transcription in target genes, occur when it binds to its nuclear receptor; however, some actions can also occur via a non-genomic signalling pathway. This review will focus on the relative importance of both pathways in the regulation of vitamin D 3-mediated UVB protection and will highlight exciting recent findings that point to new research directions.
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