(E)-4-(3,4-Dimethoxyphenyl)but-3-en-1-ol Enhances Melanogenesis through Increasing Upstream Stimulating Factor-1-Mediated Tyrosinase Expression

Jisu Park; Heesung Chung; Seung Hyun Bang; Ah-Reum Han; Eun-Kyoung Seo; Sung Eun Chang; Duk-Hee Kang; Eok-Soo Oh

doi:10.1371/journal.pone.0141988

(E)-4-(3,4-Dimethoxyphenyl)but-3-en-1-ol Enhances Melanogenesis through Increasing Upstream Stimulating Factor-1-Mediated Tyrosinase Expression

PLoS One. 2015 Nov 4;10(11):e0141988. doi: 10.1371/journal.pone.0141988. eCollection 2015.

Authors

Jisu Park¹, Heesung Chung¹, Seung Hyun Bang², Ah-Reum Han³, Eun-Kyoung Seo³, Sung Eun Chang², Duk-Hee Kang⁴, Eok-Soo Oh¹

Affiliations

¹ Department of Life Sciences, the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul, Korea.
² Department of Dermatology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea.
³ The Global Top5 Research Program, College of Pharmacy, Ewha Womans University, Seoul, Korea.
⁴ Division of Nephrology, Department of Internal Medicine, Ewha Medical Research Center, Ewha Womans University School of Medicine, Seoul, Korea.

Abstract

We investigated the potential melanogenic effect of compounds from Zingiber cassumunar Roxb. Our data revealed that chloroform-soluble extract of Z. cassumunar enhanced melanin synthesis in B16F10 melanoma cells. Among the components of the chloroform extract, (E)-4-(3,4-dimethoxyphenyl)but-3-en-1-ol (DMPB) increased melanogenesis in both B16F10 cells and human primary melanocytes. In B16F10 cells, DMPB enhanced the activation of ERK and p38, and the level of tyrosinase. Although the level of microphthalmia-associated transcription factor was unchanged in DMPB-treated B16F10 cells, DMPB increased levels and nuclear localization of upstream stimulating factor-1 (USF1). Consistently, DMPB-mediated melanin synthesis was diminished in USF1-knockdown cells. Furthermore, DMPB induced hyperpigmentation in brown guinea pigs in vivo. Together, these data suggest that DMPB may promote melanin synthesis via USF1 dependent fashion and could be used as a clinical therapeutic agent against hypopigmentation-associated diseases.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Butanols / chemistry
Butanols / isolation & purification
Butanols / pharmacology*
Cell Line, Tumor
Cell Proliferation / drug effects
Gene Expression Regulation / drug effects*
Guinea Pigs
Humans
Liquid-Liquid Extraction
Melanins / metabolism*
Melanocytes / cytology
Melanocytes / metabolism
Methanol / chemistry
Mice
Microphthalmia-Associated Transcription Factor / genetics
Microphthalmia-Associated Transcription Factor / metabolism
Microscopy, Fluorescence
Mitogen-Activated Protein Kinases / metabolism
Monophenol Monooxygenase / chemistry
Monophenol Monooxygenase / genetics
Monophenol Monooxygenase / metabolism*
Pigmentation
RNA Interference
RNA, Small Interfering / metabolism
Signal Transduction / drug effects
Upstream Stimulatory Factors / antagonists & inhibitors
Upstream Stimulatory Factors / genetics
Upstream Stimulatory Factors / metabolism*
Zingiber officinale / chemistry*
Zingiber officinale / metabolism

Substances

Butanols
Melanins
Microphthalmia-Associated Transcription Factor
RNA, Small Interfering
Upstream Stimulatory Factors
Usf1 protein, mouse
4-(3',4'-dimethoxyphenyl)but-3-en-1-ol
Monophenol Monooxygenase
Mitogen-Activated Protein Kinases
Methanol

Grants and funding

The work was supported by the following: National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIP), grant number: 2012R1A5A1048236 (URL: www.nrf.re.kr); the Korean Health Technology R&D Project, Ministry of Health & Welfare, Republic of Korea, grant number: HI12C0050 (URL: http://www.mw.go.kr); and the Ministry of Science, ICT and Future Planning (NRF2012M3A9C4048761). The funders had roles in study design, data collection and analysis, decision to publish, or preparation of the manuscript.