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Br J Ophthalmol 2004;88:566-572 doi:10.1136/bjo.2003.021204
  • Laboratory science - Extended reports

Vascular leucocyte adhesion molecules unaltered in the human retina in diabetes

  1. J M Hughes,
  2. A Brink,
  3. A N Witmer,
  4. M Hanraads-de Riemer,
  5. I Klaassen and
  6. R O Schlingemann
  1. Ocular Angiogenesis Group, Department of Ophthalmology, Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands
  1. Correspondence to: Dr R O Schlingemann Department of Ophthalmology, Academic Medical Center, Meibergdreef 15, 1105 AZ Amsterdam, Netherlands; r.schlingemannamc.uva.nl
  • Accepted 1 August 2003

Abstract

Background/aims: Capillary occlusion is believed to have a critical role in the development of diabetic retinopathy (DR). The exact mechanism by which it occurs, however, remains unclear. Several in vitro and animal model studies have suggested increased adhesion of leucocytes to the endothelium via upregulated ICAM-1 on the retinal microvasculature as a possible mechanism. In this comparative immunohistochemical study the expression of ICAM-1 was compared in the retinal vasculature of 41 eyes obtained from 37 diabetic people with 19 eyes from 19 non-diabetic controls.

Methods: Serial cryosections of postmortem posterior tissue from 41 diabetic eyes and 19 non-diabetic eyes were stained with the monoclonal antibodies ICAM-1 (two clones), CD31(panendothelial marker), and PAL-E (vascular leakage marker).

Results: A similar pattern of vascular ICAM-1 staining was observed between diabetic and non-diabetic eyes. A diffuse ICAM-1 staining of the retina was also observed that was significantly more intense in the diabetic subjects (p = 0.001).

Conclusion: These results indicate that ICAM-1 is constitutively expressed on retinal and choroidal vasculature of non-diabetic, control subjects and that this level of expression is not significantly altered by the diabetic environment. Taken together, these results do not support the prevalent paradigm of increased adhesion molecule expression as a primary mechanism responsible for capillary occlusion reported in diabetic individuals.

Notes

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