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Effects of UVA on TNF‐α, IL‐1β, and IL‐10 expression levels in human keratinocytes and intervention studies with an antioxidant and a JNK inhibitor
Author(s) -
An Li,
Dong GuoQing,
Gao Qian,
Zhang Ying,
Hu LiWen,
Li JingHai,
Liu Yang
Publication year - 2010
Publication title -
photodermatology, photoimmunology and photomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.736
H-Index - 60
eISSN - 1600-0781
pISSN - 0905-4383
DOI - 10.1111/j.1600-0781.2009.00481.x
Subject(s) - hacat , tumor necrosis factor alpha , keratinocyte , cytokine , microbiology and biotechnology , cell culture , kinase , interleukin , chemistry , biology , immunology , genetics
Objective: To understand the expressions and transduction pathways of cytokines in ultraviolet (UV)A‐irradiated keratinocytes. Methods: We cultured human keratinocytes of the HaCaT cell line and investigated both mRNA and protein expressions of cytokines in cells that were not irradiated or were exposed to 2.4 J/cm 2 UVA, with or without an antioxidant (β‐carotene) or a c‐Jun N‐terminal kinase (JNK) inhibitor (SP600125). Results: We demonstrated that the expression levels of tumor necrosis factor (TNF)‐α and interleukin (IL)‐1β were up‐regulated in irradiated cells. IL‐10 was not detected in non‐irradiated cells, but was observed in irradiated cells. JNK was activated in irradiated cells and this could be antagonized by β‐carotene. The UVA‐induced up‐regulation of these cytokines was also antagonized by β‐carotene. SP600125 inhibited the UVA‐induced increase in the expression of TNF‐α mRNA and protein and in the expression of IL‐1β mRNA. Conclusions: The results suggest that oxidative stress may be an early intermediate effect in JNK‐dependent UVA induction of cytokine expression in human keratinocytes in vitro .