Transforming growth factor-β1 decreases melanin synthesis via delayed extracellular signal-regulated kinase activation
- Authors
- Kim, Dong-Seok; Park, Seo-Hyoung; Park, Kyoung-Chan
- Issue Date
- Aug-2004
- Publisher
- PERGAMON-ELSEVIER SCIENCE LTD
- Keywords
- transforming growth factor-beta 1; melanogenesis; MITF; tyrosinase; EPK
- Citation
- INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, v.36, no.8, pp 1482 - 1491
- Pages
- 10
- Journal Title
- INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
- Volume
- 36
- Number
- 8
- Start Page
- 1482
- End Page
- 1491
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/66876
- DOI
- 10.1016/j.biocel.2003.10.023
- ISSN
- 1357-2725
1878-5875
- Abstract
- Transforming growth factor-beta1 (TGF-beta1) plays a pivotal role in cell proliferation, differentiation, and apoptosis. In this study, we investigated the effects of TGF-beta1 on melanogenesis using a spontaneously immortalized mouse melanocyte cell line, Mel-Ab. Our results show that TGF-beta1 significantly inhibits melanin synthesis in a concentration-dependent manner and that it reduces the activity of tyrosinase, the rate-limiting melanogenic enzyme. We also found that TGF-beta1 reduces microphthalmia-associated transcription factor (MITF) promoter activity and decreased MITF, tyrosinase, tyrosinase-related protein-1 (TRP-1), and TRP-2 protein production. In addition, TGF-beta1 was found to induce a delay in the activation of extracellular signal-regulated kinase (ERK) at 6 h, whereas many growth factors activate ERK transiently in minutes. Moreover, the specific ERK pathway inhibitor, PD98059 blocked the hypopigmenting effects induced by TGF-beta1. PD98059 was also found to abrogate the TGF-beta1-mediated down-regulation of MITF, tyrosinase, TRP-1, and TRP-2 production. These results suggest that the ERK pathway may be involved in the melanogenic signaling cascade, and that delayed ERK activation by TGF-beta1 contributes to reduced melanin synthesis via MITF down-regulation. (C) 2003 Elsevier Ltd. All rights reserved.
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