Abstract

Excess melanin deposition in the skin causes cosmetic problems. HSP70 upregulation decreases microphthalmia-associated transcription factor (MITF) expression, which eventually decreases tyrosinase activity and melanogenesis. Ultraviolet (UV) radiation upregulates p53, which increases the melanocortin receptor (MC1R) and MITF. Furthermore, HSP70 decreases p53 and radiofrequency irradiation (RF) increases HSP70. We evaluated whether RF increased HSP70 and decreased p53, consequently decreasing the MITF/tyrosinase pathway and melanogenesis in UV-B radiated animal skin. Various RF combinations with 50, 100, and 150 ms and 5, 10, and 15 W were performed on the UV-B radiated mouse skin every 2 d for 28 d. When RF was performed with 100 ms/10 W, melanin deposition, evaluated by Fontana–Masson staining, decreased without skin crust formation in the UV-B radiated skin. Thus, we evaluated the effect of RF on decreasing melanogenesis in the HEMn and UV-B radiated skin at a setting of 100 ms/10 W. HSP70 expression was decreased in the UV-B radiated skin but was increased by RF. The expression of p53, MC1R, and MITF increased in the UV-B radiated skin but was decreased by RF. The expression of p53, MC1R, and MITF increased in the α-MSH treated HEMn but was decreased by RF. The decreasing effects of RF on p53, MC1R, CREB and MITF were higher than those of HSP70-overexpressed HEMn. The decreasing effect of RF on p53, MC1R, CREB, and MITF disappeared in the HSP70-silenced HEMn. MC1R, CREB, and MITF were not significantly decreased by the p53 inhibitor in α-MSH treated HEMn. RF induced a greater decrease in MC1R, CREB, and MITF than the p53 inhibitor. Therefore, RF may have decreased melanin synthesis by increasing HSP70 and decreasing p53, thus decreasing MC1R/CREB/MITF and tyrosinase activity.

Highlights

  • The skin is a barrier organ which handles environmental stress and has the ability to maintain cutaneous homeostasis [1]

  • The skin pigmentation was increased by UV-B radiation, and radiofrequency irradiation (RF) decreased skin pigmentation (Figure 1B)

  • RF radiation at 50, 100, and 150 ms with 5 W showed no significant decrease in melanin accumulation compared with the UV-B group

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Summary

Introduction

The skin is a barrier organ which handles environmental stress and has the ability to maintain cutaneous homeostasis [1]. UV leads to increased activity of the local neuroendocrine system which upregulates production of various cytokines, corticotropinreleasing hormone, urocortins, proopiomelanocortin peptides, and enkephalins. Hyperpigmentation progresses in three stages in the epidermis: melanocyte proliferation, melanin production (melanogenesis) through the activation of tyrosinase, and melanosome transfer from melanocytes to keratinocytes [5,6,7,8]. Increased MITF activity leads to increased tyrosinase expression and TYRP1, which eventually increases melanin biosynthesis [21,22]. Melanogenesis by UV radiation is decreased in transgenic mice expressing HSP70 [29]. We hypothesized that RF increases HSP70, decreasing the MITF/tyrosinase pathway in UV-B radiated animal skin. Increased HSP70 might be involved in p53 modulation, which decreases MITF and melanogenesis

RF Decreased Melanin Accumulation in the UV-B Radiated Skin
RF Decreased Melanin Synthesis and Formation of Stage IV Melanosome
Skin Pigmentation Model Induced UV-B Exposure and RF Application
RF Irradiation System
In Vitro Model and RF Irradiation
Quantitative Real-Time Polymerase Chain Reaction
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