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Ultraviolet B ‐induced LGI 3 secretion protects human keratinocytes
Author(s) -
Lee Seung Hoon,
Jeong YunMi,
Kim SoYoung,
Jeong HyoSoon,
Park KyoungChan,
Baek Kwang Jin,
Kwon Nyoun Soo,
Yun HyeYoung,
Kim DongSeok
Publication year - 2012
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2012.01550.x
Subject(s) - hacat , keratinocyte , phosphorylation , secretion , ultraviolet b , protein kinase b , human skin , cancer research , microbiology and biotechnology , cell culture , chemistry , biology , immunology , medicine , endocrinology , dermatology , genetics
Leucine‐rich glioma inactivated 3 ( LGI 3) is known to be expressed mainly in the brain. However, the expression and physiological roles of LGI 3 in skin cells remain unknown. In this study, it was found for the first time that LGI 3 is expressed mostly by normal human keratinocytes. Furthermore, ELISA analysis showed that H a C a T human keratinocytes increased LGI 3 secretion after exposure to ultraviolet B ( UVB ) in a time‐ and dose‐dependent manner. We next investigated the possible role of LGI 3 in keratinocytes. LGI 3 (50 ng/ml) increased survival of H a C a T cells by 20% after UVB irradiation (150 mJ/cm 2 ). It was also found that LGI 3 stimulates the phosphorylation of A kt, which is involved in the cell survival‐signalling cascade. Furthermore, LGI 3 led to the phosphorylation of MDM 2 and subsequent p53 degradation. Taken together, the data suggest that LGI 3 may regulate p53 levels and that keratinocyte‐derived LGI 3 may act as a novel cytokine for skin homoeostasis.