Irradiance, but not fluence, plays a crucial role in UVB‐induced immature pigment cell development: new insights for efficient UVB phototherapy

Abstract

Light exposure modulates development of living organisms. In the field of medicine, light has frequently been used for regenerative purposes. Excimer light (308 nm) has demonstrated superior efficacy in treating vitiligo, a condition requiring development of melanoblasts and a model for studying nerve cell regeneration, as compared to narrow-band ultraviolet B (NBUVB; 311 nm). Using mouse-derived melanoblast cells to examine the pro-differentiation effects of these two light sources, we demonstrated that at equivalent fluence, excimer light induces melanoblast differentiation, while NBUVB failed to so. Mechanistically, activation of aryl hydrocarbon receptor pathway and nuclear translocation of epidermal growth factor receptor are involved in pro-differentiation effects of excimer light. Reduction in irradiance by filter abrogated the effects of excimer light in melanoblasts, even when equivalent fluence was delivered by the same light source. As ultraviolet B (UVB) irradiation is closely associated pigment cell development, future therapy employing UVB for pigmentation purposes should incorporate irradiance as a crucial specification.

Irradiance-dependent UVB Photocarcinogenesis

“…Alternatively, impaired CPD repair after LI UVB irradiation as compared to its HI UVB counterpart may also contribute to this phenomenon. Since our previous study already demonstrated more CPD formation immediately after LI UVB irradiation as compared to its HI UVB counterpart after equivalent exposure16, the potential impact of irradiance on DNA repair requires further investigation. It should be noted that in animal studies, after 8 weeks of regular UVB treatment, the LI UVB exposed mice skin showed higher portion of epidermal keratinocytes harboring CPD as compared to their HI UVB treated counterpart (Supplementary file Fig.…”

“…Cyclopyrimidine dimer (CPD) formation is the hallmark of DNA damage after UVB radiation and played a major role in photocarinogenesis22. Previously, we had shown that LI UVB radiation induces more CPD formation as compared to its HI counterpart if same surface exposure was administered16. Using cultured normal keratinocytes, it was found that at both 4 and 6 hrs after UVB radiation, the LI UVB treated group resulted in significantly higher CPD levels as compared to their HI UVB treated counterpart (Fig.…”

“…This scenario is similar to reduced irradiance (photon density; mW/cm 2 ) from a UVB radiation source. Intriguingly, we had recently demonstrated that UVB radiation at equivalent surface exposure (mJ/cm 2 ) but different irradiance imparts different biologic effects on immature pigment cells16. Erythema is the observed sunburn at moderate doses.…”

Role of AhR/ARNT system in skin homeostasis

“…Meanwhile, the dissociated pp60 src activates epidermal growth factor receptor (EGFR) and induces the internalization and nuclear translocation of EGFR (Fig. 1) [1, 39].

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“…UVB phototherapy is the mainstay treatment for vitiligo. A recent study by Lan et al [39] has revealed that excimer light (peak wavelength 308 nm) is more potent at inducing melanogenesis of cultured melanocytes than narrow-band UVB (peak wavelength 311 nm) because the former upregulates AhR–EGFR-dependent tyrosinase activity more efficiently than the latter.…”