Pharmaceutical & Healthcare Research Laboratories, FUJIFILM Inc., Kanagawa, Japan; Department of Applied Life Science, United Graduate School of Agricultural Science, Tokyo University of Agriculture and Technology, Tokyo, Japan.
Pharmaceutical & Healthcare Research Laboratories, FUJIFILM Inc., Kanagawa, Japan.
Biochem Biophys Res Commun. 2018 Jun 2;500(2):339-343. doi: 10.1016/j.bbrc.2018.04.070. Epub 2018 Apr 16.
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.
色素沉着的原因，如 solar lentigo 和脂溢性角化病，是黑色素在表皮基底层的过度积累。黑色素是在黑素小体中合成的，黑素小体是由基底层的黑色素细胞产生的特殊细胞器。含有黑色素的黑素小体被运输到邻近的角质形成细胞。然而，被运输到角质形成细胞后的黑素小体的行为仍知之甚少。在这项研究中，我们专注于溶酶体蛋白酶组织蛋白酶 V (CTSV)，以阐明角质形成细胞中黑素小体降解的机制。通过免疫组织化学观察，我们发现 CTSV 在正常皮肤的整个表皮中高度表达；然而，在色素沉着区域，CTSV 在基底层的表达水平低于角质层。此外，我们发现 CTSV 敲低细胞中的黑素小体降解受到抑制。这些结果表明 CTSV 参与了黑素小体的降解。
