Ultraviolet A Induces Endoplasmic Reticulum Stress Response in Human Dermal Fibroblasts

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  • Komori Ryota
    Department of Molecular Biochemistry, Graduate School of Life Science, University of Hyogo
  • Taniguchi Mai
    Department of Molecular Biochemistry, Graduate School of Life Science, University of Hyogo
  • Ichikawa Yoshiaki
    Biological Science Laboratories, Kao Corporation
  • Uemura Aya
    <orgname lang = "en">Department of Biophysics, Graduate School of Science, Kyoto University
  • Oku Masaya
    <orgname lang = "en">Department of Biophysics, Graduate School of Science, Kyoto University
  • Wakabayashi Sadao
    Department of Molecular Biochemistry, Graduate School of Life Science, University of Hyogo
  • Higuchi Kazuhiko
    Biological Science Laboratories, Kao Corporation
  • Yoshida Hiderou
    Department of Molecular Biochemistry, Graduate School of Life Science, University of Hyogo <orgname lang = "en">Department of Biophysics, Graduate School of Science, Kyoto University

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The endoplasmic reticulum (ER) stress response is a cytoprotective mechanism against the accumulation of unfolded proteins in the ER (ER stress) that consists of three response pathways (the ATF6, IRE1 and PERK pathways) in mammals. These pathways regulate the transcription of ER-related genes through specific cis-acting elements, ERSE, UPRE and AARE, respectively. Because the mammalian ER stress response is markedly activated in professional secretory cells, its main function was thought to be to upregulate the capacity of protein folding in the ER in accordance with the increased synthesis of secretory proteins. Here, we found that ultraviolet A (UVA) irradiation induced the conversion of an ER-localized sensor pATF6α(P) to an active transcription factor pATF6α(N) in normal human dermal fibroblasts (NHDFs). UVA also induced IRE1-mediated splicing of XBP1 mRNA as well as PERK-mediated phosphorylation of an α subunit of eukaryotic initiation factor 2. Consistent with these observations, we found that UVA increased transcription from ERSE, UPRE and AARE elements. From these results, we concluded that UVA irradiation activates all branches of the mammalian ER stress response in NHDFs. This suggests that the mammalian ER stress response is activated by not only intrinsic stress but also environmental stress.<br>

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