A prepared platelet-rich plasma extract, namely Self-Growth Colony, inhibits melanogenesis by down-regulating microphthalmia-associated transcription factor in skin melanocyte

Background During melanogenesis, melanocytes produce melanin through enzymatic reactions. Microphthalmia-associated transcription factor (MITF) is a major regulator in controlling the expressions of melanogenic enzymes tyrosinase (TYR), tyrosine-related protein-1 (TRP1), and dopachrome tautomerase (DCT). Self-Growth Colony (SGC) is prepared from human platelet-rich plasma (PRP) having an enrichment of growth factors, and which has claimed skin regeneration function. Aim In this study, we aim to identify and investigate the novel role of SGC in skin melanogenesis. Methods MTT assay was performed to determine the cytotoxicity of applied SGC. Melanin assay was adopted to quantify the intracellular melanin after SGC treatment. Promoter-driven luciferase assay, real-time PCR, and Western blotting were performed to determine the expressions of melanogenic enzymes and MITF in SGC-treated cultured Melan-A cells, being treated with or without UV induction. Ex vivo mouse skin was treated with SGC, and then was subjected to Western blotting and histochemical staining. Results We identified that SGC inhibited melanogenesis in cultured melanocytes and ex vivo mouse skin. The phenomena were attributed to a reduction of MITF expression, which subsequently down-regulated the melanogenic enzymes, that is, TYR, TRP1, and DCT. Moreover, ERK signaling was activated in the SGC-inhibited melanogenesis. Conclusions The findings suggest that SGC extracting from human blood can be a safe and potential agent in promoting skin whitening.

Automated summary

Recent studies have revealed that Self-Growth Colony (SGC) can inhibit melanogenesis by reducing MITF expression, leading to decreased expression of melanogenic enzymes. Additionally, SGC may achieve this effect by activating the ERK signaling pathway.