Modulation of TGF-beta 1 production from human keratinocytes by UVB

被引:59
作者
Lee, HST [1 ]
Kooshesh, F [1 ]
Sauder, DN [1 ]
Kondo, S [1 ]
机构
[1] UNIV TORONTO,SUNNYBROOK HLTH SCI CTR,DIV DERMATOL,TORONTO,ON,CANADA
关键词
inflammation; immunosuppression; cytokine; photobiology;
D O I
10.1111/j.1600-0625.1997.tb00155.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Transforming growth factor-beta (TGF-beta) plays an important role not only in cell growth control but also in inflammation and immunoregulation. There are at least five different isoforms of TGF-beta. TGF-beta 1 has a large variety of biological functions including the modulation of inflammation and the immune system and has most extensively been studied in skin. Since ultraviolet B (UVB) is known to induce skin erythema and immunosuppression, we sought to examine whether UVB would alter the expression and production of TGF-beta 1 in normal human keratinocytes. Using reverse transcription-polymerase chain reaction (RT-PCR), constitutive expression of TGF-beta 1 mRNA was detected in keratinocytes and the level of TGF-beta 1 mRNA was increased 4 and 8 h after 300 J/m(2) UVB irradiation. Production of TGF-beta 1 protein in culture supernatants assayed by ELISA was also increased at 24 h after irradiation. Cycloheximide treatment blocked this TGF-beta 1 protein induction indicating de novo protein synthesis of TGF-beta 1 from keratinocytes induced by UVB. These results suggest a possible role for TGF-beta 1 in UVB-induced skin inflammation and immunosuppression.
引用
收藏
页码:105 / 110
页数:6
相关论文
共 36 条
[21]  
MCKENZIE RC, 1994, ANN RCPSC, V27, P20
[22]  
Moller A, 1994, Exp Dermatol, V3, P314, DOI 10.1111/j.1600-0625.1994.tb00294.x
[23]   TGF-BETA STIMULATION AND INHIBITION OF CELL-PROLIFERATION - NEW MECHANISTIC INSIGHTS [J].
MOSES, HL ;
YANG, EY ;
PIETENPOL, JA .
CELL, 1990, 63 (02) :245-247
[24]  
NORRIS DA, 1993, J INVEST DERMATOL, V100, pS59
[25]  
Petrocelli T, 1996, ONCOGENE, V12, P1387
[26]   STIMULATION OF THE CHEMOTACTIC MIGRATION OF HUMAN-FIBROBLASTS BY TRANSFORMING GROWTH-FACTOR-BETA [J].
POSTLETHWAITE, AE ;
KESKIOJA, J ;
MOSES, HL ;
KANG, AH .
JOURNAL OF EXPERIMENTAL MEDICINE, 1987, 165 (01) :251-256
[27]   TRANSFORMING GROWTH FACTOR-BETA-1, A POTENT CHEMOATTRACTANT FOR HUMAN NEUTROPHILS, BYPASSES CLASSIC SIGNAL-TRANSDUCTION PATHWAYS [J].
REIBMAN, J ;
MEIXLER, S ;
LEE, TC ;
GOLD, LI ;
CRONSTEIN, BN ;
HAINES, KA ;
KOLASINSKI, SL ;
WEISSMANN, G .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (15) :6805-6809
[28]   TRANSFORMING GROWTH FACTOR-BETA-1 AND FACTOR-BETA-2 ARE MITOGENS FOR RAT SCHWANN-CELLS [J].
RIDLEY, AJ ;
DAVIS, JB ;
STROOBANT, P ;
LAND, H .
JOURNAL OF CELL BIOLOGY, 1989, 109 (06) :3419-3424
[29]   TRANSFORMING GROWTH-FACTOR TYPE-BETA - RAPID INDUCTION OF FIBROSIS AND ANGIOGENESIS INVIVO AND STIMULATION OF COLLAGEN FORMATION INVITRO [J].
ROBERTS, AB ;
SPORN, MB ;
ASSOIAN, RK ;
SMITH, JM ;
ROCHE, NS ;
WAKEFIELD, LM ;
HEINE, UI ;
LIOTTA, LA ;
FALANGA, V ;
KEHRL, JH ;
FAUCI, AS .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1986, 83 (12) :4167-4171
[30]   TARGETED DISRUPTION OF THE MOUSE TRANSFORMING GROWTH FACTOR-BETA-1 GENE RESULTS IN MULTIFOCAL INFLAMMATORY DISEASE [J].
SHULL, MM ;
ORMSBY, I ;
KIER, AB ;
PAWLOWSKI, S ;
DIEBOLD, RJ ;
YIN, MY ;
ALLEN, R ;
SIDMAN, C ;
PROETZEL, G ;
CALVIN, D ;
ANNUNZIATA, N ;
DOETSCHMAN, T .
NATURE, 1992, 359 (6397) :693-699