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Y. Kaji, S. Amano, T. Oshika, T. Usui, K. Yamashiro, S. Ishida, T. McMullen, J. Moore, A.P. Adamis, S. Horiuchi; Advanced Glycation End Products Induce Apoptosis in Corneal Endothelium . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4715.
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Purpose: The interaction of advanced glycation end products (AGEs) and AGE receptors is involved in the aging process. Recently, we reported that AGE and AGE receptors (receptor for AGE (RAGE) and galectin-3) are present in the corneal endothelium. In the present study, we investigated the effect of AGEs on the cultured bovine corneal endothelial cells (BCECs). Methods: BCECs of primary culture (2-3 passage) were used in the study. BCECs were maintained in the cultured medium containing 0 to 105 µg/ml of AGE-albumin. Uptake of AGE-albumin into BCECs was analyzed using the specific antibody to AGE. In addition, the concentration of reactive oxygen species was measured using NBT assay and the number of apoptotic cells was counted with the TUNEL staining. Results: AGE was detected in the cytoplasm of the corneal endothelial cells after incubation with the cultured medium containing AGE. In addition, AGE promoted the reactive oxygen generation and apoptosis of BCECs in dose-dependent manner.Conclusions: Corneal endothelial cells uptake AGE in the aqueous humor via specific AGE receptors. AGEs accumulate in the corneal endothelial cells by the interaction of AGE and AGE receptors, leading to apoptosis of the corneal endothelial cells. Accumulation of AGE in the corneal endothelium may play a role in the age-related loss of corneal endothelial cells.
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