The eyes of transforming growth factor-beta 1 (TGF-beta 1) transgenic mice - Morphology and the development of endotoxin-induced uveitis

被引:2
作者
Chan, CC [1 ]
Factor, V [1 ]
Li, Q [1 ]
Nagy, P [1 ]
Peng, B [1 ]
Thorgeirsson, SS [1 ]
机构
[1] NCI,EXPT CARCINOGENESIS LAB,NCI,BETHESDA,MD 20892
关键词
transforming growth factor-beta I (TGF-beta I); transgenic mouse; cataract; retinal edema; endotoxin-induced uveitis (EIU);
D O I
10.3109/09273949609079651
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Transforming growth factor-beta (TGF beta) is a potent regulator of cellular growth and immune function. The authors studied ocular histology and endotoxin-induced uveitis in a TGF-beta 1 transgenic (Tg) murine model. TGF-beta 1 Tg mice were generated by micro injecting a gene constructed by fusing the mouse albumin enhancer/promoter and porcine TGF-beta 1 cDNA. The eyes of Tg mice from two to 14 weeks of age were studied histologically. Tg mice, two to five weeks of age exhibited mild fragmentation of the lens fibers and retinal edema. No pathology was found from six to ten weeks of age, however, a progressive increased frequency of cataract was observed from 11 to 14 weeks of age. Plasma TGF-beta 1 levels were much higher in Tg mice than age-matched wild type control littermates (wt). Endotoxin-induced uveitis (EIU) in six- to eight-week-old Tg and wt mice was induced by footpad injection of lipopolysaccharide (LPS). Mice were euthanized 24 hr after LPS injection, the eyes were collected for histology and serum assayed for IL-6 and TGF-beta 1. There was a decrease in the mean numbers of infiltrating cells in Tg mice compared to wt mice. Serum IL-6 and TGF-beta 1 were much higher in Tg mice. The authors concluded that expression of the TGF-beta 1 transgene in the eyes may have effect on lens growth. Overexpression of TGF-beta 1 results in little or no effect on the development of EIU.
引用
收藏
页码:183 / 191
页数:9
相关论文
共 35 条
[1]  
ALLEN JB, 1990, J EXP MED, V177, P225
[2]  
AMIN R, 1994, INVEST OPHTH VIS SCI, V35, P3178
[3]   TRANSFORMING GROWTH-FACTOR-BETA IN DISEASE - THE DARK SIDE OF TISSUE-REPAIR [J].
BORDER, WA ;
RUOSLAHTI, E .
JOURNAL OF CLINICAL INVESTIGATION, 1992, 90 (01) :1-7
[4]   TRANSFORMING GROWTH-FACTOR BETA-1 SUPPRESSES ACUTE AND CHRONIC ARTHRITIS IN EXPERIMENTAL-ANIMALS [J].
BRANDES, ME ;
ALLEN, JB ;
OGAWA, Y ;
WAHL, SM .
JOURNAL OF CLINICAL INVESTIGATION, 1991, 87 (03) :1108-1113
[5]  
DEBOER JH, 1994, INVEST OPHTH VIS SCI, V35, P3702
[6]  
DEVOS AF, 1994, INVEST OPHTH VIS SCI, V35, P1100
[7]  
GALBREATH E, 1995, J NEUROPATHOL EXP NE, V55, P339
[8]   REGULATION OF EXPERIMENTAL AUTOIMMUNE NEURITIS BY TRANSFORMING GROWTH-FACTOR-BETA-1 [J].
GREGORIAN, SK ;
LEE, WP ;
BECK, LS ;
ROSTAMI, A ;
AMENTO, EP .
CELLULAR IMMUNOLOGY, 1994, 156 (01) :102-112
[9]   TARGETING EXPRESSION OF A TRANSFORMING GROWTH-FACTOR-BETA-1 TRANSGENE TO THE PREGNANT MAMMARY-GLAND INHIBITS ALVEOLAR DEVELOPMENT AND LACTATION [J].
JHAPPAN, C ;
GEISER, AG ;
KORDON, EC ;
BAGHERI, D ;
HENNIGHAUSEN, L ;
ROBERTS, AB ;
SMITH, GH ;
MERLINO, G .
EMBO JOURNAL, 1993, 12 (05) :1835-1845
[10]  
JOHNS LD, 1991, J IMMUNOL, V147, P1792