Open AccessMelasolv induces melanosome autophagy to inhibit pigmentation in B16F1 cells
Author(s) -
Hyun Jun Park,
Doo Sin Jo,
Hyunjung Choi,
Ji-Eun Bae,
Na Yeon Park,
Joon Bum Kim,
Ji Yeon Choi,
Yong Hwan Kim,
Gyeong Seok Oh,
Jeong Ho Chang,
Hyoung-June Kim,
DongHyung Cho
Publication year - 2020
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0239019
Subject(s) - melanosome , autophagy , microbiology and biotechnology , atg5 , melanin , bafilomycin , intracellular , biology , organelle , depigmentation , melanocyte , biochemistry , apoptosis , cancer research , melanoma , genetics
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.