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(American Journal of Pathology. 2000;156:1733-1739.)
© 2000 American Society for Investigative Pathology

Regular Articles

Vascular Endothelial Growth Factor (VEGF)-Induced Retinal Vascular Permeability Is Mediated by Intercellular Adhesion Molecule-1 (ICAM-1)

Kazuaki Miyamoto*{dagger}, Samer Khosrof*{dagger}, Sven-Erik Bursell{ddagger}, Yasufumi Moromizato*{dagger}, Lloyd Paul Aiello{ddagger}, Yuichiro Ogura§ and Anthony P. Adamis*{dagger}

From the Laboratory for Surgical Research,*
Children’s Hospital, Harvard Medical School, Boston, Massachusetts; the Department of Ophthalmology,{dagger}
Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts; the Department of Ophthalmology,{ddagger}
Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts; and the Department of Ophthalmology,§
Nagoya City University Medical School, Nagoya, Japan

Two prominent vascular endothelial growth factor (VEGF)-induced retinal effects are vascular permeability and capillary nonperfusion. The mechanisms by which these effects occur are not completely known. Using a rat model, we show that intravitreous injections of VEGF precipitate an extensive retinal leukocyte stasis (leukostasis) that coincides with enhanced vascular permeability and capillary nonperfusion. The leukostasis is accompanied by the up-regulation of intercellular adhesion molecule-1 expression in the retina. The inhibition of intercellular adhesion molecule-1 bioactivity with a neutralizing antibody prevents the permeability and leukostasis increases by 79% and 54%, respectively. These data are the first to demonstrate that a nonendothelial cell type contributes to VEGF-induced vascular permeability. Additionally, they identify a potential mechanism for VEGF-induced retinal capillary nonperfusion.




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