| Summary: | 碩士 === 國防醫學院 === 生物化學研究所 === 98 === Melanogenesis could be induced by external or environmental stimulations, provide protection from UV damage upon skin and at the same time regulate skin pigmentation. However, some factors involving the pathways of melanogenesis in associated with regulation of skin pigmentation and the mechanism of melanoma spreading remain unclear. As we know that melanogenesis would be triggered by UV irradiation through melanocytes located at the basal layer of human skin. Tyrosinase in melanosome will be activated after UV irradiation upon melanocytes followed by increasing production of melanin and transferring of melanosome to surrounding keratinocytes via dendrites of melanocytes. Recent studies showed that ion channels on cell membrane, such as TRP ion channel families, could regulate skin pigmentation and cease melanoma metastasis. However, less report focused on how ion channels regulating melanogenesis or tyrosinase activation in a normal skin model. In this work, we chose two different tyrosinase inhibitors – arbutin and kojic acid for investigating the effects on tyrosinase and TRPM1 in melanocytes. Moreover, UVA factor was added for further evaluation of the relationships of UVA, tyrosinase, and TRPM1. Our results showed that increased p53 expression and inhibition of TRPM1 were observed in melanocytes irradiated by UVA after one and two days, especially after two days. On the other hand, inhibition of TRPM1 expression was observed in the study of tyrosinase inhibitors treatment for one or two days; however, no influence on p53 was shown. In summary, it showed that UVA inhibit TRPM1 through triggering p53, while tyrosinase inhibitors exhibited inhibition effect on TRPM1 via a distinct pathway other than p53.
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