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1From the Department of Ophthalmology, University of Tokyo Graduate School of Medicine, Tokyo, Japan; the 2Department of Angiogenesis, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts; the 3Department of Ophthalmology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan; the 4Department of Ophthalmology, Teikyo University Ichihara Hospital, Chiba, Japan; and the 5Second Department of Biochemistry, University of Kumamoto School of Medicine, Kumamoto, Japan.
PURPOSE. The corneal endothelium is a target of the aging process. This study was undertaken to reveal the relationship between corneal endothelial cell (CEC) death and the accumulation of advanced glycation end products (AGEs), by investigating the possible mechanism of accumulation of AGE in CECs and its effects on CEC death.
METHODS. First, the in vivo expression of the receptor was investigated for AGE (RAGE) and galectin-3, both receptors for AGE, at both the mRNA and protein levels. Second, AGEs were added to the culture media of the cultured CECs, and the uptake of AGEs, the generation of reactive oxygen species, and the induction of apoptosis were investigated.
RESULTS. Immunohistochemistry and RT-PCR demonstrated that both RAGE and galectin-3 were expressed in bovine CECs. After administration of AGE-modified bovine serum albumin to the culture medium, uptake of AGE was observed in the cytoplasm of the cultured bovine CECs. In addition, with increasing concentration of AGEs, the generation of reactive oxygen and the number of apoptotic cells also increased.
CONCLUSIONS. These results show that the accumulation of AGEs in CECs induced apoptosis, in part, by increasing cellular oxidative stress. The accumulation of AGEs in the CECs of elderly patients may be involved in the loss of CECs during the aging process.
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