Ultraviolet A Induces Endoplasmic Reticulum Stress Response in Human Dermal Fibroblasts

Cell Structure and Function

Yoshiaki Ichikawa²  Kazuhiko Higuchi²  Mai Taniguchi¹  Sadao Wakabayashi¹  Ryota Komori¹  Aya Uemura³  Hiderou Yoshida¹  Masaya Oku³ 

[1] Department of Molecular Biochemistry, Graduate School of Life Science, University of Hyogo;Biological Science Laboratories, Kao Corporation;Department of Biophysics, Graduate School of Science, Kyoto University

关键词: ER stress;    ultraviolet A;    ATF6;    XBP1;    PERK;   

DOI  :  10.1247/csf.11041

学科分类：分子生物学，细胞生物学和基因

来源: Japan Society for Cell Biology

【 摘 要 】

References(25)Cited-By(8)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.

【 授权许可】

Unknown