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Fraxinol Stimulates Melanogenesis in B16F10 Mouse Melanoma Cells through CREB/MITF Signaling

Melanin pigment produced in melanocytes plays a protective role against ultraviolet radiation. Selective destruction of melanocytes causes chronic depigmentation conditions such as vitiligo, for which there are very few specific medical treatments. Here, we found that fraxinol, a natural coumarin fr...

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Autores principales: Moon, Sun Young, Akter, Kazi-Marjahan, Ahn, Mi-Jeong, Kim, Kwang Dong, Yoo, Jiyun, Lee, Joon-Hee, Lee, Jeong-Hyung, Hwangbo, Cheol
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8911637/
https://www.ncbi.nlm.nih.gov/pubmed/35268650
http://dx.doi.org/10.3390/molecules27051549
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author Moon, Sun Young
Akter, Kazi-Marjahan
Ahn, Mi-Jeong
Kim, Kwang Dong
Yoo, Jiyun
Lee, Joon-Hee
Lee, Jeong-Hyung
Hwangbo, Cheol
author_facet Moon, Sun Young
Akter, Kazi-Marjahan
Ahn, Mi-Jeong
Kim, Kwang Dong
Yoo, Jiyun
Lee, Joon-Hee
Lee, Jeong-Hyung
Hwangbo, Cheol
author_sort Moon, Sun Young
collection PubMed
description Melanin pigment produced in melanocytes plays a protective role against ultraviolet radiation. Selective destruction of melanocytes causes chronic depigmentation conditions such as vitiligo, for which there are very few specific medical treatments. Here, we found that fraxinol, a natural coumarin from Fraxinus plants, effectively stimulated melanogenesis. Treatment of B16-F10 cells with fraxinol increased the melanin content and tyrosinase activity in a concentration-dependent manner without causing cytotoxicity. Additionally, fraxinol enhanced the mRNA expression of melanogenic enzymes such as tyrosinase, tyrosinase-related protein-1, and tyrosinase-related protein-2. Fraxinol also increased the expression of microphthalmia-associated transcription factor at both mRNA and protein levels. Fraxinol upregulated the phosphorylation of cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB). Furthermore, H89, a cAMP–dependent protein kinase A inhibitor, decreased fraxinol-induced CREB phosphorylation and microphthalmia-associated transcription factor expression and significantly attenuated the fraxinol-induced melanin content and intracellular tyrosinase activity. These results suggest that fraxinol enhances melanogenesis via a protein kinase A-mediated mechanism, which may be useful for developing potent melanogenesis stimulators.
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spelling pubmed-89116372022-03-11 Fraxinol Stimulates Melanogenesis in B16F10 Mouse Melanoma Cells through CREB/MITF Signaling Moon, Sun Young Akter, Kazi-Marjahan Ahn, Mi-Jeong Kim, Kwang Dong Yoo, Jiyun Lee, Joon-Hee Lee, Jeong-Hyung Hwangbo, Cheol Molecules Article Melanin pigment produced in melanocytes plays a protective role against ultraviolet radiation. Selective destruction of melanocytes causes chronic depigmentation conditions such as vitiligo, for which there are very few specific medical treatments. Here, we found that fraxinol, a natural coumarin from Fraxinus plants, effectively stimulated melanogenesis. Treatment of B16-F10 cells with fraxinol increased the melanin content and tyrosinase activity in a concentration-dependent manner without causing cytotoxicity. Additionally, fraxinol enhanced the mRNA expression of melanogenic enzymes such as tyrosinase, tyrosinase-related protein-1, and tyrosinase-related protein-2. Fraxinol also increased the expression of microphthalmia-associated transcription factor at both mRNA and protein levels. Fraxinol upregulated the phosphorylation of cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB). Furthermore, H89, a cAMP–dependent protein kinase A inhibitor, decreased fraxinol-induced CREB phosphorylation and microphthalmia-associated transcription factor expression and significantly attenuated the fraxinol-induced melanin content and intracellular tyrosinase activity. These results suggest that fraxinol enhances melanogenesis via a protein kinase A-mediated mechanism, which may be useful for developing potent melanogenesis stimulators. MDPI 2022-02-25 /pmc/articles/PMC8911637/ /pubmed/35268650 http://dx.doi.org/10.3390/molecules27051549 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Moon, Sun Young
Akter, Kazi-Marjahan
Ahn, Mi-Jeong
Kim, Kwang Dong
Yoo, Jiyun
Lee, Joon-Hee
Lee, Jeong-Hyung
Hwangbo, Cheol
Fraxinol Stimulates Melanogenesis in B16F10 Mouse Melanoma Cells through CREB/MITF Signaling
title Fraxinol Stimulates Melanogenesis in B16F10 Mouse Melanoma Cells through CREB/MITF Signaling
title_full Fraxinol Stimulates Melanogenesis in B16F10 Mouse Melanoma Cells through CREB/MITF Signaling
title_fullStr Fraxinol Stimulates Melanogenesis in B16F10 Mouse Melanoma Cells through CREB/MITF Signaling
title_full_unstemmed Fraxinol Stimulates Melanogenesis in B16F10 Mouse Melanoma Cells through CREB/MITF Signaling
title_short Fraxinol Stimulates Melanogenesis in B16F10 Mouse Melanoma Cells through CREB/MITF Signaling
title_sort fraxinol stimulates melanogenesis in b16f10 mouse melanoma cells through creb/mitf signaling
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8911637/
https://www.ncbi.nlm.nih.gov/pubmed/35268650
http://dx.doi.org/10.3390/molecules27051549
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