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

被引:6
|
作者
Iwata, Masahiro [1 ,2 ]
Kawahara, Ko-ichi [1 ]
Kawabata, Hisashi [2 ]
Ito, Takashi [1 ]
Mera, Kentaro [2 ]
Biswas, Kamal Krishna [1 ]
Tancharoen, Salunya [3 ]
Higashi, Yuko [2 ]
Kikuchi, Kiyoshi [1 ]
Hashiguchi, Teruto [1 ]
Kanekura, Takuro [2 ]
Maruyama, Ikuro [1 ]
机构
[1] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Cardiovasc & Resp Disorders Adv Therapeut, Lab Vasc Med, Kagoshima 8908520, Japan
[2] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Dermatol, Kagoshima 8908520, Japan
[3] Mahidol Univ, Fac Dent, Dept Pharmacol, Bangkok 10400, Thailand
关键词
Thrombomodulin; UVB; p38MAPK; HaCaT cells;
D O I
10.1016/j.bbrc.2008.10.049
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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(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. (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:642 / 647
页数:6
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