한빛사논문
- 조회223
Ki Won Lee 1, Yong-Yeon Cho 2, Kwang Dong Kim 1 3 4 *
1ABC-RLRC, Gyeongsang National University, Jinju, South Korea.
2College of Pharmacy, The Catholic University of Korea, Bucheon-si, Gyeonggi-Do, Korea.
3Division of Applied Life Science (BK21 Four), Gyeongsang National University, Jinju, South Korea.
4PMBBRC, Gyeongsang National University, Jinju, South Korea.
*Corresponding author: correspondence to Kwang Dong Kim
Abstract
Dysregulation of melanin homeostasis is implicated in causing skin pigmentation disorders, such as melasma due to hyperpigmentation and vitiligo due to hypopigmentation. Although the synthesis of melanin has been well studied, the removal of the formed skin pigment requires more research. We determined that β-mangostin, a plant-derived metabolite, induces the degradation of already-formed melanin in the mouse B16F10 cell line. The whitening effect of β-mangostin is mediated by macroautophagy/autophagy, as it was abolished by the knockdown of ATG5 or RB1CC1/FIP200, and by treatment with 3-methyladenine, a phosphatidylinositol 3-kinase complex inhibitor. However, the exact autophagy mechanism of melanosome degradation remains unknown. Selective autophagy for a specific cellular organelle requires specific E3-ligases and autophagic receptors for the target organelle. In this study, an E3-ligase, RCHY1, and an autophagy receptor, OPTN (optineurin), were identified as being essential for melanophagy in the β-mangostin-treated B16F10 cell line. As per our knowledge, this is the first report of a specific mechanism for the degradation of melanosomes, the target organelle of melanophagy. These findings are expected to broaden the scope of melanin homeostasis research and can be exploited for the development of therapeutics for skin pigmentation disorders.
논문정보
- Research article
- 2024년 06월 (BRIC 등록일 2024-07-17)
- 국내 연구진
- 생명과학 > 세포생물학
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