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Qian Yang, Marina V Yasvoina, Meidong Zhu, Marcus Fruttiger; Gliovascular alterations in the retina from a diabetic patient without diabetic retinopathy. Invest. Ophthalmol. Vis. Sci. 2018;59(9):3551.
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© ARVO (1962-2015); The Authors (2016-present)
Astrocytes and Müller cells are macroglial cells in the retina that form gliovascular units with retinal vessels. Intact and functional gliovascular units are important in providing metabolic support for retinal neurons and regulating osmostasis. Here we present a case study demonstrating gliovascular unit disruption in specific retinal layers in a post-mortem diabetic eye.
Post-mortem ocular tissues were obtained from Moorfields Eye Bank (London, UK) and Lions NSW Eye Bank (Sydney, Australia). Whole mounts of eight eyes from diabetic patients and three from the control group were stained with Ulex Europaeus Agglutinin (UEA) to visualise the vasculature. These were then embedded in paraffin and sectioned (6μm). Retinal mapping was generated by using the distribution of major blood vessels within a section to pinpoint its position in the whole mount image. A diabetic donor eye with no apparent vascular pathology was chosen for further investigation and compared to healthy controls. Sections were immunostained with antibodies against neuronal (NSE, opsin and rhodopsin), glial (Aquaporin4, Crystallin αA, CRALBP, GFAP, Glutamine Synthetase and Vimentin) and vascular (Collagen and UAE) markers.
In the diabetic retina, the nerve fibre layer was thickened in the periphery, but not in the centre of the retina. Lack of Aquaporin4 (AQP4) expression was observed in gliovascular units in within the thickened regions of the nerve fibre layer. The associated astrocytes presented an abnormally ramified morphology. Avascular capillaries were found in all regions of the retina, but their incidence was significantly higher in the deep versus the superficial vascular plexus in the same eye, as well as in the control eyes.
The abnormal AQP4 distribution observed in our diabetic sample suggests disturbed osmostasis in the nerve fibre layer, and is likely to represent an early phenotype diabetes induced retinal pathology. Similarly, the vascular dropout specifically in the deeper vascular plexus is likely to be diabetes related. In summary, our case study suggests that AQP4 mislocalisation and endothelial cell loss in the deeper plexus may be markers of early diabetic retinopathy, although further specimens will need to be studied.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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