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PLoS One. 2016 Dec 12;11(12):e0168025. doi: 10.1371/journal.pone.0168025. eCollection 2016.

Primary Cilia Negatively Regulate Melanogenesis in Melanocytes and Pigmentation in a Human Skin Model.

Author information

1
Department of Gerontology, Graduate School of East-West Medical Science, Kyung Hee University, Yongin, Gyeonggi-do, Republic of Korea.
2
R&D Unit, AmorePacific Corporation, Yongin, Gyeonggi-do, Republic of Korea.
3
Department of Medical Science, Korea University Ansan Hospital, Ansan, Gyeonggi-do, Republic of Korea.
4
Biomedical Research Institute, MEDIPOST Corporation, Seongnam, Gyeonggi-do, Republic of Korea.
5
Department of Pharmacology, Wonju College of Medicine, Yonsei University, Wonju, Gangwon-do, Republic of Korea.

Abstract

The primary cilium is an organelle protruding from the cell body that senses external stimuli including chemical, mechanical, light, osmotic, fluid flow, and gravitational signals. Skin is always exposed to the external environment and responds to external stimuli. Therefore, it is possible that primary cilia have an important role in skin. Ciliogenesis was reported to be involved in developmental processes in skin, such as keratinocyte differentiation and hair formation. However, the relation between skin pigmentation and primary cilia is largely unknown. Here, we observed that increased melanogenesis in melanocytes treated with a melanogenic inducer was inhibited by a ciliogenesis inducer, cytochalasin D, and serum-free culture. However, these inhibitory effects disappeared in GLI2 knockdown cells. In addition, activation of sonic hedgehog (SHH)-smoothened (Smo) signaling pathway by a Smo agonist, SAG inhibited melanin synthesis in melanocytes and pigmentation in a human skin model. On the contrary, an inhibitor of primary cilium formation, ciliobrevin A1, activated melanogenesis in melanocytes. These results suggest that skin pigmentation may be regulated partly by the induction of ciliogenesis through Smo-GLI2 signaling.

PMID:
27941997
PMCID:
PMC5152889
DOI:
10.1371/journal.pone.0168025
[Indexed for MEDLINE]
Free PMC Article

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