Solar ultraviolet radiation as a trigger of cell signal transduction

被引:104
作者
Heck, DE
Gerecke, DR
Vetrano, AM
Laskin, JD
机构
[1] UMDNJ, Robert Wood Johnson Med Sch, Dept Environm & Community Med, Piscataway, NJ 08854 USA
[2] Rutgers State Univ, Dept Pharmacol & Toxicol, Piscataway, NJ 08854 USA
关键词
UVB; UVA; MAP kinase; skin cancer; melanoma;
D O I
10.1016/j.taap.2003.09.028
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Ultraviolet light radiation in sunlight is known to cause major alterations in growth and differentiation patterns of exposed human tissues. The specific effects depend on the wavelengths and doses of the light, and the nature of the exposed tissue. Both growth inhibition and proliferation are observed, as well as inflammation and immune suppression. Whereas in the clinical setting, these responses may be beneficial, for example, in the treatment of psoriasis and atopic dermatitis, as an environmental toxicant, ultraviolet light can induce significant tissue damage. Thus, in the eye, ultraviolet light causes cataracts, while in the skin, it induces premature aging and the development of cancer. Although ultraviolet light can damage many tissue components including membrane phospholipids, proteins, and nucleic, acids, it is now recognized that many of its cellular effects arc due to alterations in growth factor- and cytokine-mediated signal transduction pathways leading to aberrant gene expression. It is generally thought that reactive oxygen intermediates are mediators of some of the damage induced by ultraviolet light. Generated when ultraviolet light is absorbed by endogenous photosensitizers in the presence of molecular oxygen, reactive oxygen intermediates and their metabolites induce damage by reacting with cellular electrophiles, some of which can directly initiate cell signaling processes. In an additional layer of complexity, ultraviolet light-damaged nucleic acids initiate signaling during the activation of repair processes. Thus, mechanisms by which solar ultraviolet radiation triggers cell signal transduction are multifactorial. The present review summarizes some of the mechanisms by which ultraviolet light alters signaling pathways as well as the genes important in the beneficial and toxic effects of ultraviolet light. (C) 2003 Elsevier Inc. All rights reserved.
引用
收藏
页码:288 / 297
页数:10
相关论文
共 157 条
[91]  
MURPHY GM, 1989, PHOTODERMATOLOGY, V6, P268
[92]   Mitogen-activated protein kinases mediate peroxynitrite-induced cell death in human bronchial epithelial cells [J].
Nabeyrat, E ;
Jones, GE ;
Fenwick, PS ;
Barnes, PJ ;
Donnelly, LE .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2003, 284 (06) :L1112-L1120
[93]   Polymorphisms in the TNF region confer susceptibility to UVB-induced impairment of contact hypersensitivity induction in mice and humans [J].
Niizeki, H ;
Inoko, H ;
Streilein, JW .
METHODS, 2002, 28 (01) :46-54
[94]   Polymorphisms in the tumor necrosis factor (TNF) genes are associated with susceptibility to effects of ultraviolet-B radiation on induction of contact hypersensitivity [J].
Niizeki, H ;
Naruse, T ;
Hecker, KH ;
Taylor, JR ;
Kurimoto, I ;
Shimizu, T ;
Yamasaki, Y ;
Inoko, H ;
Streilein, JW .
TISSUE ANTIGENS, 2001, 58 (06) :369-378
[95]   The role of ultraviolet irradiation and heparin-binding epidermal growth factor-like growth factor in the pathogenesis of pterygium [J].
Nolan, TM ;
DiGirolamo, N ;
Sachdev, NH ;
Hampartzoumian, T ;
Coroneo, MT ;
Wakefield, D .
AMERICAN JOURNAL OF PATHOLOGY, 2003, 162 (02) :567-574
[96]   Mitogen and stress-activated protein kinase 1 mediates activation of Akt by ultraviolet B irradiation [J].
Nomura, M ;
Kaji, A ;
Ma, WY ;
Zhong, SP ;
Liu, GM ;
Bowden, CT ;
Miyamoto, K ;
Dong, ZG .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (27) :25558-25567
[97]   Studies to determine the immunomodulating effects of cis-urocanic acid [J].
Norval, M ;
El-Ghorr, AA .
METHODS, 2002, 28 (01) :63-70
[98]   Ultraviolet-B-induced oxidative DNA base damage in primary normal human epidermal keratinocytes and inhibition by a hydroxyl radical scavenger [J].
Pelle, E ;
Huang, X ;
Mammone, T ;
Marenus, K ;
Maes, D ;
Frenkel, K .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2003, 121 (01) :177-183
[99]   The CD95(APO-1/Fas) DISC and beyond [J].
Peter, ME ;
Krammer, PH .
CELL DEATH AND DIFFERENTIATION, 2003, 10 (01) :26-35
[100]   H2O2 is an important mediator of UVB-induced EGF-receptor phosphorylation in cultured keratinocytes [J].
Peus, D ;
Vasa, RA ;
Meves, A ;
Pott, M ;
Beyerle, A ;
Squillace, K ;
Pittelkow, MR .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1998, 110 (06) :966-971