Abstract
Ultraviolet (UV)-associated hyperpigmented skins are characterized with increased vasculature underlying pigmentation, suggestive of the possible biological role of endothelial cells in the regulation of skin pigmentation during UV irradiation. In this study, we showed that UV-irradiated endothelial cells significantly increased the pigmentation of melanocytes through epithelial-mesenchymal crosstalk. The stimulatory effect of endothelial cells was further demonstrated using ex vivo human skin. RNA sequence analysis and enzyme-linked immunosorbent assay showed that endothelial cells secrete more stem cell factor (SCF) upon UV irradiation than non-irradiated cells. The increased pigmentation elicited by endothelial cells was abrogated following inhibition of SCF/c-KIT signaling. Together these results suggest that endothelial cells are activated upon UV exposure to release melanogenic factors such as SCF, which contributes to the development of skin hyperpigmentation during chronic sun exposure.
Highlights
The strategic location of the skin as the barrier between the environment and internal milieu determines its critical function in the preservation of body homeostasis, and organism survival[1]
The results showed that melanin levels and tyrosinase activity were significantly increased in melanocytes treated with conditioned medium (CM) from UV-human dermal microvascular endothelial cells (HDMECs) as compared with the control cells (Fig. 1b, Supplementary Fig. S1)
An increase in pigmentation was observed in melanocytes treated with CM from HDMECs irradiated with 50 mJ/ cm[2] UVB, UVB is known to reach only the endothelial cells located at the superficial dermis level under physiological conditions (Fig. 1d, Supplementary Fig. S3)
Summary
The strategic location of the skin as the barrier between the environment and internal milieu determines its critical function in the preservation of body homeostasis, and organism survival[1]. UV-irradiated fibroblasts produce stem cell factor (SCF) or secreted frizzled-related protein-2 (sFRP2), which influence melanogenesis and play a role in pigmentation of observed in solar lentigo or melasma[8,9,10]. The increased vasculature was thought to be a consequence of UV irradiation, as the hyperpigmented skin displayed more prominent solar elastosis and increased expression of vascular endothelial growth factor (VEGF), a major angiogenic factor of UV-irradiated skin, as compared with the perilesional normal skin. These findings suggest that the changes in dermal endothelial cells resulting from chronic sun exposure may cause melanocytes to synthesize melanin in the epidermis. We investigated the crosstalk between UV-irradiated endothelial cells and melanocytes
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