Lens epithelial, cell apoptosis is an early event in the development of UVB-induced cataract

被引:170
作者
Li, WC [1 ]
Spector, A [1 ]
机构
[1] COLUMBIA UNIV COLL PHYS & SURG, DEPT OPHTHALMOL, BIOCHEM & MOLEC BIOL LAB, NEW YORK, NY 10032 USA
关键词
UVB irradiation; generation of free radicals; lens; cataract; epithelium; cell apoptosis; cell viability; c-fos; DNA fragmentation; free radicals;
D O I
10.1016/0891-5849(96)02050-3
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
Epidemiological and experimental studies have revealed that exposure to UV can induce cataractogenesis. To investigate the mechanism of this induction, viability of the lens epithelial cells from UVB-treated rat lenses were examined. Irradiation of the cultured rat lenses with 8 J/s/m(2) UVB for 60 min triggers lens epithelial cell apoptosis as determined by terminal deoxyribonucleotide transferase (TdT) labeling and DNA fragmentation assays. The apoptotic lens epithelial cells were initially found in the equatorial region and then quickly appeared in both equatorial and central regions. The percentage of apoptotic cells continuously increased during the postirradiation incubation. After a 5-h post-UVB incubation, more than 50% of the lens epithelial cells were apoptotic. By 24 h, all of the lens epithelial cells in the irradiated lenses were dead through apoptosis. Associated with this apoptotic process is a large upregulation of the proto-oncogene, c-fos. Opacification appears to follow the death of lens epithelial cells occurring first in the equatorial region and then in the central area. This is also true of classical cataract parameters such as non-protein thiol and wet weight, which are significantly modified only after appreciable epithelial cell apoptosis. Together, these results suggest that the rapid apoptotic death of the lens epithelial cells induced by UVB initiates cataract development.
引用
收藏
页码:301 / 311
页数:11
相关论文
共 83 条
[22]   A TECHNIQUE FOR RADIOLABELING DNA RESTRICTION ENDONUCLEASE FRAGMENTS TO HIGH SPECIFIC ACTIVITY [J].
FEINBERG, AP ;
VOGELSTEIN, B .
ANALYTICAL BIOCHEMISTRY, 1983, 132 (01) :6-13
[23]   INDIRECT MECHANISMS OF HIV PATHOGENESIS - HOW DOES HIV KILL T-CELLS [J].
FINKEL, TH ;
BANDA, NK .
CURRENT OPINION IN IMMUNOLOGY, 1994, 6 (04) :605-615
[24]   HUMAN CLUSTERIN GENE-EXPRESSION IS CONFINED TO SURVIVING CELLS DURING IN-VITRO PROGRAMMED CELL-DEATH [J].
FRENCH, LE ;
WOHLWEND, A ;
SAPPINO, AP ;
TSCHOPP, J ;
SCHIFFERLI, JA .
JOURNAL OF CLINICAL INVESTIGATION, 1994, 93 (02) :877-884
[25]   IDENTIFICATION OF PROGRAMMED CELL-DEATH INSITU VIA SPECIFIC LABELING OF NUCLEAR-DNA FRAGMENTATION [J].
GAVRIELI, Y ;
SHERMAN, Y ;
BENSASSON, SA .
JOURNAL OF CELL BIOLOGY, 1992, 119 (03) :493-501
[26]   UVB-INDUCED DNA BREAKS INTERFERE WITH TRANSCRIPTIONAL INDUCTION OF C-FOS [J].
GHOSH, R ;
AMSTAD, P ;
CERUTTI, P .
MOLECULAR AND CELLULAR BIOLOGY, 1993, 13 (11) :6992-6999
[27]   APOPTOSIS IN AIDS [J].
GOUGEON, ML ;
MONTAGNIER, L .
SCIENCE, 1993, 260 (5112) :1269-1270
[28]   UNSCHEDULED DNA-REPAIR IN HUMAN LENS EPITHELIUM FOLLOWING INVIVO AND INVITRO ULTRAVIOLET-IRRADIATION [J].
GRABNER, G ;
BRENNER, W .
OPHTHALMIC RESEARCH, 1982, 14 (03) :160-166
[29]   ACTIVATION-INDUCED DEATH BY APOPTOSIS IN CD4+ T-CELLS FROM HUMAN-IMMUNODEFICIENCY-VIRUS INFECTED ASYMPTOMATIC INDIVIDUALS [J].
GROUX, H ;
TORPIER, G ;
MONTE, D ;
MOUTON, Y ;
CAPRON, A ;
AMEISEN, JC .
JOURNAL OF EXPERIMENTAL MEDICINE, 1992, 175 (02) :331-340
[30]  
Harding J.J., 1984, EYE B, P207