Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.] · 2013
Epidermal growth factor and epidermal growth factor signaling attenuate laser-induced melanogenesis.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Yun Woo Jin, Bang Seung Hyun, Min Kyung Hyun, Kim Seong Who, Lee Mi Woo, Chang Sung Eun
Аннотация
BACKGROUND: Epidermal growth factor (EGF) is a peptide that promotes cell growth by binding to its receptor (EGFR) on the cell surface. EGF has been used in cosmetics to whiten the skin and for the prevention of postinflammatory hyperpigmentation (PIH), presumably by accelerating wound healing, but the effects of EGF on melanogenesis are not known, and the presence of EGFR on melanocytes has not been confirmed.
METHODS: To establish a role of EGF in melanogenesis, we first investigated expression of EGFR on melanocytes. Second, in the search for an effect of EGF on PIH, we investigated the effect of EGF on melanin production by melanocytes with or without laser-treated keratinocyte-conditioned culture media (LCM).
RESULTS: Treatment with EGF did not affect proliferation of melan-A, mouse-derived immortalized melanocytes. Melanocytes treated with LCM had greater prostaglandin-E2 (PGE2) expression and tyrosinase enzyme activity than melanocytes treated with control media. Treatment with EGF lowered melanin production of LCM-treated melanocytes but not of melanocytes treated with control media.
CONCLUSION: Our results support EGF as a candidate target for development of antimelanogenic agents in PIH.
METHODS: To establish a role of EGF in melanogenesis, we first investigated expression of EGFR on melanocytes. Second, in the search for an effect of EGF on PIH, we investigated the effect of EGF on melanin production by melanocytes with or without laser-treated keratinocyte-conditioned culture media (LCM).
RESULTS: Treatment with EGF did not affect proliferation of melan-A, mouse-derived immortalized melanocytes. Melanocytes treated with LCM had greater prostaglandin-E2 (PGE2) expression and tyrosinase enzyme activity than melanocytes treated with control media. Treatment with EGF lowered melanin production of LCM-treated melanocytes but not of melanocytes treated with control media.
CONCLUSION: Our results support EGF as a candidate target for development of antimelanogenic agents in PIH.