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Alistair J. Barber, David A. Antonetti, Thomas W. Gardner, The Penn State Retina Research Group; Altered Expression of Retinal Occludin and Glial Fibrillary Acidic Protein in Experimental Diabetes. Invest. Ophthalmol. Vis. Sci. 2000;41(11):3561-3568.
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purpose. To investigate how diabetes alters vascular endothelial cell tight
junction protein and glial cell morphology at the blood–retinal
methods. The distribution of the glial marker, glial fibrillary acidic protein
(GFAP), and the endothelial cell tight junction protein occludin were
explored by immunofluorescence histochemistry in flatmounted retinas of
streptozotocin (STZ)-diabetic and age-matched control rats, and in
BB/Wor diabetes-prone and age-matched diabetes-resistant rats.
results. GFAP immunoreactivity was limited to astrocytes in control retinas. Two
months of STZ-diabetes reduced GFAP immunoreactivity in astrocytes and
increased GFAP immunoreactivity in small groups of Müller cells.
After 4 months of STZ-induced diabetes, all Müller cells had
intense GFAP immunoreactivity, whereas there was virtually none in the
astrocytes. BB/Wor diabetic rats had similar changes in GFAP
immunoreactivity. Occludin immunoreactivity in normal rats was greatest
in the capillary bed of the outer plexiform layer and arterioles of the
inner retina but much less intense in the postcapillary venules.
Diabetes reduced occludin immunoreactivity in the capillaries and
induced redistribution from continuous cell border to interrupted,
punctate immunoreactivity in the arterioles. Forty-eight hours of
insulin treatment reversed the pattern of GFAP and occludin
immunoreactivity in the STZ-diabetic rats.
conclusions. Diabetes alters GFAP expression in retinal glial cells, accompanied by
reduction and redistribution of occludin in endothelial cells. These
changes are consistent with the concept that altered glial–endothelial
cell interactions at the BRB contribute to diabetic retinopathy.
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