Changes of MMP-1 and collagen type Iα1 by UVA, UVB and IRA are differentially regulated by Trx-1

被引:80
作者
Buechner, Nicole [1 ]
Schroeder, Peter [1 ]
Jakob, Sascha [1 ]
Kunze, Kerstin [1 ]
Maresch, Tanja [1 ]
Calles, Christian [1 ]
Krutmann, Jean [1 ]
Haendeler, Judith [1 ]
机构
[1] Univ Dusseldorf gGmbH, IUF, D-40225 Dusseldorf, Germany
关键词
aging; thioredoxin-1; UV light; infrared; metalloproteinase-1; collagen;
D O I
10.1016/j.exger.2008.04.009
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Exposure of human skin to solar radiation, which includes ultraviolet (UV) radiation (UVA and UVB) visible light and infrared radiation, induces skin aging. The effects of light have been attributed to irradiation-induced reactive oxygen species (ROS) formation, but the specific signaling pathways are not well understood. Detrimental effects of solar radiation are dermal diseases and photoaging. Exposure of cultured human dermal fibroblasts to UVA, UVB or IRA increased ROS formation in vitro. One important redox regulator is the oxidoreductase thioredoxin-1 (Trx). Trx is ubiquitously expressed and has anti-oxidative and anti-apoptotic properties. Besides its function to reduce H2O2, Trx binds to and regulates transcription factors. The aim of this study was to investigate whether Trx influences the regulation of MMP-1 and collagen I alpha 1 by UVA, UVB and IRA. We irradiated human dermal fibroblasts with UVA, UVB and IRA. UVA, UVB and IRA upregulated MMP-1 expression. Trx inhibited UVA-induced MMP-1 upregulation in a NF kappa B dependent manner. UVA, UVB and IRA reduced collagen I alpha 1 expression. Incubation with Trx inhibited the effects of UVB and IRA on collagen lot] expression. In conclusion, MMP-1 and collagen I alpha 1, which play important roles in aging processes, seems to be regulated by different transcriptional mechanisms and Trx can only influence distinct signaling pathways induced by UVA, UVB and probably IRA. Thus, Trx may serve as an important contributor to an "anti-aging therapeutic cocktail". (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:633 / 637
页数:5
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