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Tailoi Chan-Ling, Samyoul Ahn, Mark Koina, Mohammad Nasir Uddin, Ted Maddess, Samuel Adamson, Marconi Barbosa; Changes in the Radial Peri-papillary Capillaries (RPCs) in human retina during ‘physiological aging’: the forgotten vascular bed in glaucoma pathogenesis. Invest. Ophthalmol. Vis. Sci. 2017;58(8):3391.
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© ARVO (1962-2015); The Authors (2016-present)
To characterize the structure, distribution, caliber & glial ensheathment of radial peri-papillary capillaries (RPCs) in human retina & their changes during ‘physiological aging’.
A total of 53 human eyes including 1 young (aged 9) and 52 adults (aged 17-84) were examined. Multiple marker immunohistochemistry was performed with markers CD34, CD39, GFAP, NG2, α-SMA, S-100b, NF, Neu-N and UEA-1 Lectin to examine vascular density, astrocyte & pericyte ensheathement, RPC distribution, vascular branching patterns and CD39 expression levels. RPCs ultrastructure was examined using TEM.
RPCs are located within 6μm of the inner limiting membrane and have unique ultrastructural features including thin basal lamina, sparse astrocyte & pericyte ensheathment, and importantly, luminal diameter of 4-5μm as compared to capillaries in the superficial vascular plexus. The outer limit of RPCs extended significantly further than previously reported by Henkind (1967) & showed a higher anastomosis, suggesting higher perfusion efficiency in healthy young adults. Mapping of the outer limit of the RPCs & quantitative morphological analysis in 48 adult retinas showed that their extent, caliber & vessel density decreased significantly with age. CD39 expression intensity & vascular density were also found to decrease. Importantly, not only did the extent & density of RPCs decrease with age, many RPC segments showed marked decrease in caliber with some segments appearing collapsed, suggestive of a compromised rheology. Vessel caliber showed a decrease from 7-7.5μm in healthy young adults to 6μm in the 8th decade.
The superficial location and thin basal lamina of RPCs make them susceptible to lumen collapse under high intraocular pressure, while their restriction to the nerve fiber layer makes them responsible for the metabolic needs of the ganglion cell axons, making their functional capacity particularly relevant to glaucoma pathogenesis. Further, CD39 plays a major role in ATP-dependent processes as well as preventing thrombotic & inflammatory processes. The significant reduction in CD39 expression will further compromise RPCs function during ‘physiological aging’. These findings are supportive of the utility of quantitative analysis of RPCs as an indicator of glaucoma predisposition, requiring further study in glaucomatous population.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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