Tranexamic acid may promote melanocores clustering in keratinocytes through upregulation of Rab5b

Tranexamic acid (TXA) is a promising therapeutic agent in melasma that can act on multiple pathophysiologic mechanisms of melasma. However, it is unclear whether TXA affects melanin in keratinocytes. To explore the effect of TXA on melanocores in keratinocytes. The melanocore‐incorporated keratinocy...

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Bibliographic Details
Published in:Experimental dermatology 2023-06, Vol.32 (6), p.777-786
Main Authors: Hu, Yebei, Chen, Yi, Zhao, Yan, Geng, Qingwei, Guan, Cuiping, Xu, Jinhui, Xie, Bo, Song, Xiuzu
Format: Article
Language:English
Subjects:
Autophagy
Electrons
Keratinocytes
Melanin
melanocore
melasma
Protein transport
Proteins
Rab5b
tranexamic acid
Transcriptomes
Transmission electron microscopy
Up-regulation
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Summary:Tranexamic acid (TXA) is a promising therapeutic agent in melasma that can act on multiple pathophysiologic mechanisms of melasma. However, it is unclear whether TXA affects melanin in keratinocytes. To explore the effect of TXA on melanocores in keratinocytes. The melanocore‐incorporated keratinocytes were constructed by co‐incubating normal human epidermal keratinocytes (NHEK) with melanocores. After being treated with TXA, autophagy‐ and melanin‐related protein expressions were detected. Then, transcriptome sequencing was used to compare the genetic changes in melanocore‐incorporated keratinocytes before and after TXA treatment and further verified the differentially expressed genes. At the same time, the distribution of melanocores in human keratinocytes was observed by transmission electron microscopy. We found that TXA does not promote melanin degradation in primary keratinocytes by inducing autophagy. Protein transport and intracellular protein transport‐related genes were enriched after TXA treatment, and Rab5b was significantly upregulated. Transmission electron microscopy showed that the percentage of melanocores distributed in clusters increased after treatment with TXA, which was reduced after Rab5b silencing. In addition, results suggested that melanocores could colocalize with Rab5b and lysosome‐associated membrane protein1 (LAMP1). Our study found that Rab5b may be involved in the melanocore distribution in keratinocytes. TXA may promote the clustering distribution of endocytic melanocores through upregulation of Rab5b, representing a potential mechanism of TXA treatment against melasma.
ISSN:0906-6705
1600-0625
DOI:10.1111/exd.14767