Exposure of human skin to solar ultraviolet radiation (UVR), a powerful carcinogen comprising ~95% UVA wavelengths (320-400 nm) and 5% UVB wavelengths (280-320 nm) at the Earth’s surface, promotes synthesis of melanin pigment in epidermal melanocytes, which protects skin from DNA damage. Exposure to UVB causes DNA lesions that lead to activation of repair mechanisms and transcriptional activation of melanin-producing enzymes, resulting in delayed skin pigmentation within days. In contrast, UVA causes primarily oxidative damage and leads to immediate pigment darkening within minutes of exposure via an unknown mechanism. Though many organisms use dermal photoreception mechanisms to mediate a range of behaviours, no receptor protein directly mediating photoreception in human skin has been identified. <br/><br/> This work demonstrates the expression of opsins, light-sensitive G-protein coupled receptors, in human epidermal melanocytes and shows that their activation by exposure to UVA causes calcium mobilization and early melanin synthesis. Calcium responses were abolished by treatment with G protein or PLC inhibitors, or by depletion of intracellular calcium stores. Upon UVA exposure, significant melanin production was measured within one hour; cellular melanin continued to increase in a retinal- and calcium-dependent manner up to five-fold after 24 hours. This work identifies a novel UVA-sensitive dermal photosensing pathway in melanocytes that leads to calcium mobilization and early melanin synthesis, and may underlie the elusive mechanism of immediate pigment darkening in human skin.<br/><br/>
Wicks, Nadine L.,
"Ultraviolet Light Phototransduction in Human Skin"
(2012).
Molecular Pharmacology, Physiology, and Biotechnology Theses and Dissertations.
Brown Digital Repository. Brown University Library.
https://doi.org/10.7301/Z0BZ64B7
