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S Ishida, K Yamashiro, T Usui, Y Kaji, E Ahmed, AP Adamis; ICAM-1 Blockade Leads to Suppression of Retinal Leukostasis in Established Diabetes . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1325.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To compare the effect of intercellular adhesion molecule-1 (ICAM-1) blockade on retinal leukostasis in early and established diabetes. Methods: The retinal vasculature and adherent leukocytes were imaged with FITC-conjugated Concanavalin A (Con A) lectin in streptozotocin-induced diabetic rats. Immunohistochemistry for CD45 (leukocyte common antigen) was performed in the retinal flat mounts. Neutralizing antibodies against rat ICAM-1 were administered via intraperitoneal injection to block leukocyte adhesion to the retinal vasculature. Results: Immunohistochemistry confirmed that the Con A lectin stained cells within the retinal vasculature were positive for CD45. Compared to non-diabetic animals (29.3±10.1 leukocytes/retina, n=6), retinal leukostasis increased two-fold in 2-week (early) diabetic rats (61.4±10.9, n=6, p<0.05) and five-fold in 3-month (established) diabetes (155.1±33.3, n=6, p<0.05). Treatment with an anti-ICAM-1 antibody resulted in 93% blockade of early diabetic retinal leukostasis (31.4±17.3, n=6, p<0.05) and 71% of established diabetic retinal leukostasis (65.6±34.7, n=6, p<0.05). Conclusion: Retinal leukostasis increases with the duration of diabetes. An anti-ICAM-1 therapeutic approach has beneficial effects on retinal leukostasis in both early and established diabetes.
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