Ultraviolet B irradiation decreases CXCL10 expression in keratinocytes through endoplasmic reticulum stress

Tomokazu Ohnishi, Mitsuhiro Hisadome, Kusuyama Joji, Norika Chiba, Muhammad Subhan Amir, Takuro Kanekura, Tetsuya Matsuguchi

Research output: Contribution to journalArticlepeer-review

Abstract

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 H2O2 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.

Original languageEnglish
Pages (from-to)1141-1156
Number of pages16
JournalJournal of Cellular Biochemistry
Volume122
Issue number9
DOIs
Publication statusPublished - 2021 Sep

Keywords

  • CXCL10
  • ER stress
  • IFN-γ
  • keratinocytes
  • STAT1
  • UVB

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Fingerprint

Dive into the research topics of 'Ultraviolet B irradiation decreases CXCL10 expression in keratinocytes through endoplasmic reticulum stress'. Together they form a unique fingerprint.

Cite this