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Glabridin Promotes Melanosome Degradation and Alleviates Melanosome-Induced Mitochondrial Dysfunction in Keratinocytes via Autophagy

ABSTRACT: Background: The excessive accumulation of melanosomes within keratinocytes contributes to skin hyperpigmentation and disrupts normal epidermal proliferation. Glabridin, an isoflavone derived from Glycyrrhiza glabra L., is a potent skin-lightening agent with tyrosinase-inhibitory activity. This study aims to further elucidate the skin-lightening mechanism of glabridin by investigating its effects on melanosome degradation. Methods: We investigated the effect of glabridin on melanosome degradation by measuring melanin content and PMEL17 protein levels. Autophagy activity was evaluated by mRNA sequencing, Western blot, and immunofluorescence. In vivo depigmenting efficacy was examined using epidermal skin equivalents and zebrafish embryos. Additionally, ATP content and mitochondrial membrane potential were measured to determine whether glabridin ameliorates melanosome-induced mitochondrial dysfunction. Results: Glabridin promoted melanosome degradation in keratinocytes and exhibited depigmenting effects in both pigmented epidermal skin equivalents and zebrafish embryos. Mechanistically, glabridin activated autophagy, and pharmacological inhibition of autophagy blocked its depigmenting effects. Additionally, we found that melanosome accumulation impaired mitochondrial function in keratinocytes, an effect that was reversed by glabridin. Conclusions: These findings demonstrate that glabridin promotes melanosome degradation via autophagy activation, which is associated with improved mitochondrial function, providing mechanistic insight into its skin-lightening effects.

ORGANISM(S): Homo sapiens

PROVIDER: GSE327103 | GEO | 2026/04/06

REPOSITORIES: GEO

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Project description:Epidermis, a continuously self-renewing and differentiating organ, produces a protective stratum corneum that shields us from external chemical, physical and microbial threats. Epidermal differentiation is a multi-step process regulated by influences, some unknown, others insufficiently explored. Detachment of keratinocytes from the basement membrane is one such pro-differentiation stimulus. Here, we define the transcriptional changes during differentiation, especially those caused by detachment from the substratum. Using comprehensive transcriptional profiling, we revisited the effects of detachment as a differentiation signal to keratinocytes. We identified the genes regulated by detachment, the corresponding ontological categories and, using metaanalysis, compared the genes and categories to those regulated by other pro-differentiating stimuli. We identified 762 genes overexpressed in suspended keratinocyte, including known and novel differentiation markers, and 1427 in attached cells, including basal layer markers. Detachment induced epidermis development, cornification and desmosomal genes, but also innate immunity, proliferation inhibitors, transcription regulators and MAPKs; conversely the attached cells overexpressed cell cycle, anchoring, motility, splicing and mitochondrial genes, and both positive and negative regulators of apoptosis. Metaanalysis identified which detachment-regulated categories overlap with those induced by suprabasal location in vivo, by reaching confluency in vitro, and by inhibition of JUN kinases. Attached and in vivo basal cells shared overexpression of mitochondrial components. Interestingly, melanosome trafficking components were also overexpressed in the attached and in vivo basal keratinocytes. Reaching confluency did not affect adhesion and ECM proteins. Lipid metabolism and steroid metabolism were induced by confluency and by JNK inhibition, respectively. These results suggest that specific pro-differentiation signals induce specific features of the keratinization process, which are in vivo orchestrated into harmonious epidermal homeostasis. Human epidermal keratinocytes are grown in standard growth medium either attached in tissue culture plates, or suspended, in the same medium, in bacteriological plates. After 48 hrs, attached and suspended cultures were harvested and their transcriptomes compared.

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Glabridin Promotes Melanosome Degradation and Alleviates Melanosome-Induced Mitochondrial Dysfunction in Keratinocytes via Autophagy

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