Ursolic acid inhibits pigmentation by increasing melanosomal autophagy in B16F1 cells

Melanosomes are specialized membrane-bound organelles that are involved in melanin synthesis. Unlike melanosome biogenesis, the melanosome degradation pathway is poorly understood. Among the cellular processes, autophagy controls degradation of intracellular components by cooperating with lysosomes....

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Published in:Biochemical and biophysical research communications 2020-10, Vol.531 (2), p.209-214
Main Authors: Park, Hyun Jun, Jo, Doo Sin, Choi, Dong Sig, Bae, Ji-Eun, Park, Na Yeon, Kim, Jun-Bum, Chang, Jeong Ho, Shin, Joong Jin, Cho, Dong-Hyung
Format: Article
Language:English
Subjects:
alpha-MSH - pharmacology
Animals
Autophagy
Autophagy - drug effects
B16F1 cells
Cell Line, Tumor
Melanins - biosynthesis
Melanoma, Experimental - pathology
Melanophagy
Melanosome
Melanosomes - drug effects
Melanosomes - pathology
Mice
Skin Pigmentation - drug effects
TPC2
Triterpenes - chemistry
Triterpenes - pharmacology
Ursolic Acid
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Summary:Melanosomes are specialized membrane-bound organelles that are involved in melanin synthesis. Unlike melanosome biogenesis, the melanosome degradation pathway is poorly understood. Among the cellular processes, autophagy controls degradation of intracellular components by cooperating with lysosomes. In this study, we showed that ursolic acid inhibits skin pigmentation by promoting melanosomal autophagy, or melanophagy, in melanocytes. We found that B16F1 cells treated with ursolic acid suppressed alpha-melanocyte stimulating hormone (α-MSH) stimulated increase in melanin content and activated autophagy. In addition, we found that treatment with ursolic acid promotes melanosomal degradation, and bafilomycin A1 inhibition of autophagosome–lysosome fusion blocked the removal of melanosomes in α-MSH-stimulated B16F1 cells. Furthermore, depletion of the autophagy-related gene 5 (ATG5) resulted in significant suppression of ursolic acid–mediated anti-pigmentation activity and autophagy in α-MSH-treated B16F1 cells. Taken together, our results suggest that ursolic acid inhibits skin pigmentation by increasing melanosomal degradation in melanocytes. •Ursolic acid suppressed the α-MSH-stimulated increase of melanin contents.•Ursolic acid increased the autophagic flux of melanosome, whereas combination with bafilomycin A1 suppressed their degradation in B16F1 cells.•Depletion of ATG5 blocked ursolic acid-mediated depigmentation and autophagy in α-MSH-treated cells.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2020.07.125