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Melasolv induces melanosome autophagy to inhibit pigmentation in B16F1 cells

The melanosome is a specialized membrane-bound organelle that is involved in melanin synthesis, storage, and transportation. In contrast to melanosome biogenesis, the processes underlying melanosome degradation remain largely unknown. Autophagy is a process that promotes degradation of intracellular...

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Detalles Bibliográficos
Autores principales: Park, Hyun Jun, Jo, Doo Sin, Choi, Hyunjung, Bae, Ji-Eun, Park, Na Yeon, Kim, Joon Bum, Choi, Ji Yeon, Kim, Yong Hwan, Oh, Gyeong Seok, Chang, Jeong Ho, Kim, Hyoung-June, Cho, Dong-Hyung
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7498095/
https://www.ncbi.nlm.nih.gov/pubmed/32941497
http://dx.doi.org/10.1371/journal.pone.0239019
Descripción
Sumario:The melanosome is a specialized membrane-bound organelle that is involved in melanin synthesis, storage, and transportation. In contrast to melanosome biogenesis, the processes underlying melanosome degradation remain largely unknown. Autophagy is a process that promotes degradation of intracellular components’ cooperative process between autophagosomes and lysosomes, and its role for process of melanosome degradation remains unclear. Here, we assessed the regulation of autophagy and its contributions to depigmentation associated with Melasolv (3,4,5-trimethoxycinnamate thymol ester). B16F1 cells-treated with Melasolv suppressed the α-MSH-stimulated increase of melanin content and resulted in the activation of autophagy. However, introduction of bafilomycin A1 strongly suppressed melanosome degradation in Melasolv-treated cells. Furthermore, inhibition of autophagy by ATG5 resulted in significant suppression of Melasolv-mediated depigmentation in α-MSH-treated cells. Taken together, our results suggest that treatment with Melasolv inhibits skin pigmentation by promoting melanosome degradation via autophagy activation.