May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Advanced Glycation End Products Induce Apoptosis in Corneal Endothelium
Author Affiliations & Notes
  • Y. Kaji
    Department of Ophthalmology, Univ of Tsukuba Institute of Clinical Science, Tsukuba-shi, Japan
  • S. Amano
    Department of Ophthalmology, Univ of Tokyo Graduate School of Medicine, Hongo 7-3-1, Japan
  • T. Oshika
    Department of Ophthalmology, Univ of Tokyo Graduate School of Medicine, Hongo 7-3-1, Japan
  • T. Usui
    Department of Ophthalmology, Univ of Tokyo Graduate School of Medicine, Hongo 7-3-1, Japan
  • K. Yamashiro
    Department of Ophthalmology, University of Kyoto Graduate School of Medicine, Tsukuba-shi, Japan
  • S. Ishida
    Department of Ophthalmology, Keio University School of Medicine, Tsukuba-shi, Japan
  • T. McMullen
    Immunology, University of Ulster School of Biomedical Sciences, Tsukuba-shi, Ireland
  • J. Moore
    Department of Ophthalmology, The Queen's University of Belfast, Belfast, Ireland
  • A.P. Adamis
    Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, MA, United States
  • S. Horiuchi
    Department of Biochemistry, Univ of Kumamoto School of Medicine, Kumamoto-shi, Japan
  • Footnotes
    Commercial Relationships  Y. Kaji, None; S. Amano, None; T. Oshika, None; T. Usui, None; K. Yamashiro, None; S. Ishida, None; T. McMullen, None; J. Moore, None; A.P. Adamis, None; S. Horiuchi, None.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 4715. doi:
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    • Get Citation

      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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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : 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.

Keywords: cornea: endothelium • apoptosis/cell death • aging 
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