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Title: ER signaling is activated to protect human HaCaT keratinocytes from ER stress induced by environmental doses of UVB

Abstract

Proteins are folded properly in the endoplasmic reticulum (ER). Various stress such as hypoxia, ischemia and starvation interfere with the ER function, causing ER stress, which is defined by the accumulation of unfolded protein (UP) in the ER. ER stress is prevented by the UP response (UPR) and ER-associated degradation (ERAD). These signaling pathways are activated by three major ER molecules, ATF6, IRE-1 and PERK. Using HaCaT cells, we investigated ER signaling in human keratinocytes irradiated by environmental doses of ultraviolet B (UVB). The expression of Ero1-L{alpha}, an upstream signaling molecule of ER stress, decreased at 1-4 h after 10 mJ/cm{sup 2} irradiation, indicating that the environmental dose of UVB-induced ER stress in HaCaT cells, without growth retardation. Furthermore, expression of intact ATF6 was decreased and it was translocated to the nuclei. The expression of XBP-1, a downstream molecule of IRE-1, which is an ER chaperone whose expression is regulated by XBP-1, and UP ubiquitination were induced by 10 mJ/cm{sup 2} UVB at 4 h. PERK, which regulates apoptosis, was not phosphorylated. Our results demonstrate that UVB irradiation generates UP in HaCaT cells and that the UPR and ERAD systems are activated to protect cells from UVB-induced ER stress. Thismore » is the first report to show ER signaling in UVB-irradiated keratinocytes.« less

Authors:
 [1];  [2]; ;  [1]; ;  [2];  [1]
  1. Department of Dermatology, Field of Sensory Organology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890-8520 (Japan)
  2. Department of Laboratory and Vascular Medicine Cardiovascular and Respiratory Disorders Advanced Therapeutics, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890-8520 (Japan)
Publication Date:
OSTI Identifier:
22202667
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 397; Journal Issue: 2; Other Information: Copyright (c) 2010 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRONMENTAL POLLUTANT EFFECTS ON LIVING ORGANISMS AND BIOLOGICAL MATERIALS; ANOXIA; APOPTOSIS; BIOLOGICAL RADIATION EFFECTS; ENDOPLASMIC RETICULUM; IRRADIATION; ISCHEMIA; PROTEINS; RADIATION DOSES; ULTRAVIOLET RADIATION

Citation Formats

Mera, Kentaro, Kawahara, Ko-ichi, Tada, Ko-ichi, Kawai, Kazuhiro, Hashiguchi, Teruto, Maruyama, Ikuro, and Kanekura, Takuro. ER signaling is activated to protect human HaCaT keratinocytes from ER stress induced by environmental doses of UVB. United States: N. p., 2010. Web. doi:10.1016/J.BBRC.2010.05.128.
Mera, Kentaro, Kawahara, Ko-ichi, Tada, Ko-ichi, Kawai, Kazuhiro, Hashiguchi, Teruto, Maruyama, Ikuro, & Kanekura, Takuro. ER signaling is activated to protect human HaCaT keratinocytes from ER stress induced by environmental doses of UVB. United States. https://doi.org/10.1016/J.BBRC.2010.05.128
Mera, Kentaro, Kawahara, Ko-ichi, Tada, Ko-ichi, Kawai, Kazuhiro, Hashiguchi, Teruto, Maruyama, Ikuro, and Kanekura, Takuro. 2010. "ER signaling is activated to protect human HaCaT keratinocytes from ER stress induced by environmental doses of UVB". United States. https://doi.org/10.1016/J.BBRC.2010.05.128.
@article{osti_22202667,
title = {ER signaling is activated to protect human HaCaT keratinocytes from ER stress induced by environmental doses of UVB},
author = {Mera, Kentaro and Kawahara, Ko-ichi and Tada, Ko-ichi and Kawai, Kazuhiro and Hashiguchi, Teruto and Maruyama, Ikuro and Kanekura, Takuro},
abstractNote = {Proteins are folded properly in the endoplasmic reticulum (ER). Various stress such as hypoxia, ischemia and starvation interfere with the ER function, causing ER stress, which is defined by the accumulation of unfolded protein (UP) in the ER. ER stress is prevented by the UP response (UPR) and ER-associated degradation (ERAD). These signaling pathways are activated by three major ER molecules, ATF6, IRE-1 and PERK. Using HaCaT cells, we investigated ER signaling in human keratinocytes irradiated by environmental doses of ultraviolet B (UVB). The expression of Ero1-L{alpha}, an upstream signaling molecule of ER stress, decreased at 1-4 h after 10 mJ/cm{sup 2} irradiation, indicating that the environmental dose of UVB-induced ER stress in HaCaT cells, without growth retardation. Furthermore, expression of intact ATF6 was decreased and it was translocated to the nuclei. The expression of XBP-1, a downstream molecule of IRE-1, which is an ER chaperone whose expression is regulated by XBP-1, and UP ubiquitination were induced by 10 mJ/cm{sup 2} UVB at 4 h. PERK, which regulates apoptosis, was not phosphorylated. Our results demonstrate that UVB irradiation generates UP in HaCaT cells and that the UPR and ERAD systems are activated to protect cells from UVB-induced ER stress. This is the first report to show ER signaling in UVB-irradiated keratinocytes.},
doi = {10.1016/J.BBRC.2010.05.128},
url = {https://www.osti.gov/biblio/22202667}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 2,
volume = 397,
place = {United States},
year = {Fri Jun 25 00:00:00 EDT 2010},
month = {Fri Jun 25 00:00:00 EDT 2010}
}