April 1992
Volume 33, Issue 5
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Articles  |   April 1992
Freeze-fracture and lanthanum studies of the retinal microvasculature in diabetic rats.
Author Affiliations
  • R B Caldwell
    Department of Cellular Biology and Anatomy, The Medical College of Georgia, Augusta 30912.
  • S M Slapnick
    Department of Cellular Biology and Anatomy, The Medical College of Georgia, Augusta 30912.
Investigative Ophthalmology & Visual Science April 1992, Vol.33, 1610-1619. doi:
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      R B Caldwell, S M Slapnick; Freeze-fracture and lanthanum studies of the retinal microvasculature in diabetic rats.. Invest. Ophthalmol. Vis. Sci. 1992;33(5):1610-1619.

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Abstract

To see whether or not blood-retinal barrier breakdown during diabetes was associated with breakdown of the endothelial cell tight junctions or with other membrane alterations in the cells comprising the wall of the retinal microvasculature, streptozotocin-induced diabetic rat retinas were studied using lanthanum tracer and freeze-fracture electron microscopic morphometry. This study showed that endothelial cell tight junction permeability to lanthanum and luminal surface area were normal in these diabetic rats. However, freeze-fracture morphometry showed several alterations in the diabetic retinal microvessels. First, the endothelial cell membranes had abnormally large (80-120 nm) plasmalemmal vesicles not evident in the control retinas, suggesting that membrane turnover was abnormal. Second, endothelial cell P-face membranes at the blood front contained more larger particles than those in the control rats (P less than 0.05), implying an alteration in endothelial cell luminal membrane composition. Third, endothelial cell P-face membranes in areas of close apposition with pericyte membranes showed abnormal areas of particle clearing not seen in the control animals, suggesting a change in pericyte-endothelial cell interactions. Finally, pericyte membranes facing the neural retina contained increased numbers of plasmalemmal vesicles compared with control membranes (P less than 0.05). Moreover, the association of these vesicles with collagen fibrils in the extracellular space suggested an alteration in extracellular matrix turnover.

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