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Ultraviolet B irradiation decreases CXCL10 expression in keratinocytes through endoplasmic reticulum stress
Author(s) -
Ohnishi Tomokazu,
Hisadome Mitsuhiro,
Joji Kusuyama,
Chiba Norika,
Amir Muhammad Subhan,
Kanekura Takuro,
Matsuguchi Tetsuya
Publication year - 2021
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29936
Subject(s) - hacat , cxcl10 , endoplasmic reticulum , keratinocyte , unfolded protein response , psoriasis , microbiology and biotechnology , cell culture , chemistry , biology , chemokine , immunology , receptor , biochemistry , genetics
Ultraviolet radiation is one of the standard treatment selections for psoriasis. interferon (IFN)‐γ and IFN‐γ‐induced CXCL10, which are highly expressed by keratinocytes in psoriasis lesion, are therapeutic targets for psoriasis. In this study, we found that ultraviolet B (UVB) irradiation inhibited IFN‐γ signaling events, including STAT1 phosphorylation and induction of CXCL10 messenger RNA (mRNA) expression in keratinocytes. IFN‐γ‐induced expression of CXCL10 mRNA in HaCaT cells, a human keratinocyte cell line, and human epithelial keratinocytes were also inhibited by H 2 O 2 or endoplasmic reticulum (ER) stress inducers. Conversely, a mixture of antioxidants, Trolox and ascorbic acid, and the ER stress inhibitor salubrinal partially counteracted the inhibitory effect of UVB on IFN‐γ‐induced CXCL10 mRNA expression in HaCaT cells. We also found that UVB and ER stress reduced IFN‐γ receptor 1 protein levels in the plasma membrane fraction of keratinocytes. These observations suggested that ER stress and the generation of reactive oxygen species are essential for the inhibitory effect of UVB on IFN‐γ‐induced CXCL10 mRNA in keratinocytes.