December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
ICAM-1 Blockade Leads to Suppression of Retinal Leukostasis in Established Diabetes
Author Affiliations & Notes
  • S Ishida
    Angiogenesis/Retina Research Laboratory Massachusetts Eye & Ear Infirmary Harvard Medical School Boston MA
  • K Yamashiro
    Angiogenesis/Retina Research Laboratory Massachusetts Eye & Ear Infirmary Harvard Medical School Boston MA
  • T Usui
    Angiogenesis/Retina Research Laboratory Massachusetts Eye & Ear Infirmary Harvard Medical School Boston MA
  • Y Kaji
    Angiogenesis/Retina Research Laboratory Massachusetts Eye & Ear Infirmary Harvard Medical School Boston MA
  • E Ahmed
    Angiogenesis/Retina Research Laboratory Massachusetts Eye & Ear Infirmary Harvard Medical School Boston MA
  • AP Adamis
    Angiogenesis/Retina Research Laboratory Massachusetts Eye & Ear Infirmary Harvard Medical School Boston MA
  • Footnotes
    Commercial Relationships   S. Ishida, None; K. Yamashiro, None; T. Usui, None; Y. Kaji, None; E. Ahmed, None; A.P. Adamis, None.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 1325. doi:
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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)

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Abstract

Abstract: : 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.

Keywords: 388 diabetic retinopathy • 339 cell adhesions/cell junctions • 506 pathology: experimental 
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