skip to main content
OSTI.GOV title logo U.S. Department of Energy
Office of Scientific and Technical Information

Title: Thrombomodulin exerts cytoprotective effect on low-dose UVB-irradiated HaCaT cells

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [2];  [1];  [2];  [1];  [2];  [3];  [4]; ;  [5]
  1. Department of Dermatology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890-8520 (Japan)
  2. Laboratory of Vascular Medicine, Department of Cardiovascular and Respiratory Disorders Advanced Therapeutics, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890-8520 (Japan)
  3. Department of Pharmacology, Faculty of Dentistry, Mahidol University, Bangkok 10400 (Thailand)
  4. Dept. of Dermatology, Kagoshima Univ. Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890-8520 (Japan)
  5. Lab. of Vascular Medicine, Dept. of Cardiovascular and Respiratory Disorders Advanced Therapeutics, Kagoshima Univ. Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890-8520 (Japan)

Thrombomodulin (TM) is an endothelial cell surface anticoagulant glycoprotein that performs antimetastatic, angiogenic, adhesive, and anti-inflammatory functions in various tissues. It is also expressed in epidermal keratinocytes. We found that a physiological dose (10 mJ/cm{sup 2}) of mid-wavelength ultraviolet irradiation (UVB) significantly induced TM expression via the p38mitogen-activated protein kinase (MAPK)/cyclic AMP response element (CRE) signaling pathway in the epidermal keratinocyte cell line HaCaT; this shows that TM regulates the survival of HaCaT cells. SB203580, a p38MAPK inhibitor, significantly decreased TM expression and the viability of cells exposed to UVB. Furthermore, overexpression of TM markedly increased cell viability, and it was abrogated by TM small interfering RNA (siRNA), suggesting that TM may play an important role in exerting cytoprotective effect on epidermal keratinocytes against low-dose UVB.

OSTI ID:
21255788
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 377, Issue 2; Other Information: DOI: 10.1016/j.bbrc.2008.10.049; PII: S0006-291X(08)01999-2; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

Similar Records

NF-κB-dependent transcriptional upregulation of cyclin D1 exerts cytoprotection against hypoxic injury upon EGFR activation
Journal Article · Sat Sep 10 00:00:00 EDT 2016 · Experimental Cell Research · OSTI ID:21255788

ER signaling is activated to protect human HaCaT keratinocytes from ER stress induced by environmental doses of UVB
Journal Article · Fri Jun 25 00:00:00 EDT 2010 · Biochemical and Biophysical Research Communications · OSTI ID:21255788

Expression of VEGFR-2 on HaCaT cells is regulated by VEGF and plays an active role in mediating VEGF induced effects
Journal Article · Fri Oct 13 00:00:00 EDT 2006 · Biochemical and Biophysical Research Communications · OSTI ID:21255788