Melanosome degradation in epidermal keratinocytes related to lysosomal protease cathepsin V
The cause of hyperpigmentation, such as solar lentigo and seborrheic keratosis, is the excessive accumulation of melanin pigments in the epidermal basal layer. Melanin pigments are synthesized in the melanosomes, which are specific organelles produced by melanocytes in the basal layer. Melanosomes c...
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Published in | Biochemical and biophysical research communications Vol. 500; no. 2; pp. 339 - 343 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
02.06.2018
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Subjects | |
Online Access | Get full text |
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Summary: | The cause of hyperpigmentation, such as solar lentigo and seborrheic keratosis, is the excessive accumulation of melanin pigments in the epidermal basal layer. Melanin pigments are synthesized in the melanosomes, which are specific organelles produced by melanocytes in the basal layer. Melanosomes containing melanin pigments are transported to the neighboring keratinocytes. However, the behavior of melanosomes after being transported to the keratinocytes has been poorly understood.
In this study, we focused on a lysosomal protease cathepsin V (CTSV) to clarify the mechanism underlying melanosome degradation in the keratinocytes. Using immunohistochemical observation, we found that CTSV was highly expressed across the entire epidermis in normal skin; however, CTSV expression levels were lower in the basal layer than those in the stratum corneum side in the hyperpigmented region. Moreover, we found that melanosome degradation was suppressed in CTSV knockdown cells. These results indicated that CTSV is involved in melanosome degradation.
•Final destination of melanosomes after transportation to keratinocytes is poorly understood.•Majority of melanosomes is present in the basal layer of epidermis.•Cathepsin V may be involved in melanosome degradation. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2018.04.070 |