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Epidermal Platelet‐activating Factor Receptor Activation and Ultraviolet B Radiation Result in Synergistic Tumor Necrosis Factor‐alpha Production
Author(s) -
Wolverton Jay E.,
AlHassani Mohammed,
Yao Yongxue,
Zhang Qiwei,
Travers Jeffrey B.
Publication year - 2010
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.2009.00618.x
Subject(s) - tumor necrosis factor alpha , cytokine , platelet activating factor , protein kinase c , platelet activating factor receptor , agonist , phorbol , receptor , cancer research , chemistry , microbiology and biotechnology , biology , immunology , signal transduction , biochemistry , antagonist
Ultraviolet B radiation (UVB) is a potent stimulator of epidermal cytokine production which has been implicated in photoaggravated dermatoses. In addition to cytokines such as tumor necrosis factor‐α (TNF‐α), UVB generates bioactive lipids including platelet‐activating factor (PAF). Our previous studies have demonstrated that UVB‐mediated production of keratinocyte TNF‐α is in part due to PAF. The current studies use a human PAF‐receptor (PAF‐R) negative epithelial cell line transduced with PAF‐Rs and PAF–R‐deficient mice to demonstrate that activation of the epidermal PAF‐R along with UVB irradiation results in a synergistic production of TNF‐α. It should be noted that PAF‐R effects are mimicked by the protein kinase C (PKC) agonist phorbol myristic acetate, and are inhibited by pharmacological antagonists of the PKC gamma isoenzyme. These studies suggest that concomitant PAF‐R activation and UVB irradiation results in a synergistic production of the cytokine TNF‐α which is mediated in part via PKC. These studies provide a novel potential mechanism for photosensitivity responses.