Abstract
Autophagy is involved in the degradation of melanosomes and the determination of skin color. TLR4 and tumor necrosis factor (TNF) signaling upregulates NF-kB expression, which is involved in the upregulation of mTOR. The activation of mTOR by UV-B exposure results in decreased autophagy, whereas radiofrequency (RF) irradiation decreases TLR4 and TNF receptor (TNFR) expression. We evaluated whether RF decreased skin pigmentation by restoring autophagy by decreasing the expression of TLR4 or TNFR/NF-κB/mTOR in the UV-B-irradiated animal model. UV-B radiation induced the expressions of TNFR, TLR, and NF-κB in the skin, which were all decreased by RF irradiation. RF irradiation also decreased phosphorylated mTOR expression and upregulated autophagy initiation factors such as FIP200, ULK1, ULK2, ATG13, and ATG101 in the UV-B-irradiated skin. Beclin 1 expression and the expression ratio of LC3-I to LC3-II were increased by UV-B/RF irradiation. Furthermore, melanin-containing autophagosomes increased with RF irradiation. Fontana-Masson staining showed that the amount of melanin deposition in the skin was decreased by RF irradiation. This study showed that RF irradiation decreased skin pigmentation by restoring melanosomal autophagy, and that the possible signal pathways which modulate autophagy could be TLR4, TNFR, NF-κB, and mTOR.
Highlights
Melanin is a nitrogen-containing pigment made from the melanin precursor L-tyrosine and is deposited in melanosomes, which are subcellular lysosome-like organelles [1]
We evaluated whether RF irradiation decreased the expressions of TNF receptor (TNFR), TLR4, and NF-κB in the UV-B-irradiated human primary epidermal keratinocytes (HEKn cells)
The expressions of TNFR, TLR4, and NF-κB were significantly increased by UV-B radiation in Human primary epidermal keratinocytes (HEKn) cells, whereas RF irradiation significantly decreased them at 24 h after RF
Summary
Melanin is a nitrogen-containing pigment made from the melanin precursor L-tyrosine and is deposited in melanosomes, which are subcellular lysosome-like organelles [1] Both keratinocytes and melanocytes are involved in melanogenesis in the skin: melanocytes produce the melanin and deliver it to the keratinocytes for skin protection [2]. UV-B-irradiated keratinocytes secrete high-mobility group box 1 (HMGB1), which is a ligand of TLR4 [21] These proteins are associated with post-inflammatory hyperpigmentation, which results from the overproduction or irregular dispersion of melanin [22]. RF could decrease skin pigmentation by modulating skin inflammation through the downregulation of various pro-inflammatory signals like NF-κB, TNF-α, and TLR4. It is well known that UV-B irradiation increases various inflammatory cytokines and increases NF-κB, which eventually decreases melanosomal autophagy and increases skin pigmentation. We investigated the effects of RF irradiation on autophagy and skin pigmentation in the UV-B radiation animal model
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
