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Research Article Free access | 10.1172/JCI1277

Advanced glycation end products increase retinal vascular endothelial growth factor expression.

M Lu, M Kuroki, S Amano, M Tolentino, K Keough, I Kim, R Bucala, and A P Adamis

Laboratory for Surgical Research, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

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Laboratory for Surgical Research, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

Find articles by Kuroki, M. in: JCI | PubMed | Google Scholar

Laboratory for Surgical Research, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

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Laboratory for Surgical Research, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

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Laboratory for Surgical Research, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

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Laboratory for Surgical Research, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

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Laboratory for Surgical Research, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

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Laboratory for Surgical Research, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

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Published March 15, 1998 - More info

Published in Volume 101, Issue 6 on March 15, 1998
J Clin Invest. 1998;101(6):1219–1224. https://doi.org/10.1172/JCI1277.
© 1998 The American Society for Clinical Investigation
Published March 15, 1998 - Version history
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Abstract

Advanced glycation end products (AGEs) are linked with the development of diabetic retinopathy; however, the pathogenic mechanisms are poorly defined. Vascular endothelial growth factor (VEGF) levels are increased in ischemic and nonischemic diabetic retina, and VEGF is required for the development of retinal and iris neovascularization. Moreover, VEGF alone can induce much of the concomitant pathology of diabetic retinopathy. In this study, we found that AGEs increased VEGF mRNA levels in the ganglion, inner nuclear, and retinal pigment epithelial (RPE) cell layers of the rat retina. In vitro, AGEs increased VEGF mRNA and secreted protein in human RPE and bovine vascular smooth muscle cells. The AGE-induced increases in VEGF expression were dose- and time-dependent, inhibited by antioxidants, and additive with hypoxia. Use of an anti-VEGF antibody blocked the capillary endothelial cell proliferation induced by the conditioned media of AGE-treated cells. AGEs may participate in the pathogenesis of diabetic retinopathy through their ability to increase retinal VEGF gene expression.

Version history
  • Version 1 (March 15, 1998): No description
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