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Rhonda Grebe, Irum Mughal, William Bryden, Jing Tian, Malia Michelle Edwards, Scott McLeod, Gregory S Hageman, Gerard A Lutty; Analysis of choriocapillaris ultrastructure in macular regions of eyes obtained from patients with neovascular AMD, geographic atrophy, and pure one and ten chromosomal abnormalities. Invest. Ophthalmol. Vis. Sci. 2017;58(8):2260.
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© ARVO (1962-2015); The Authors (2016-present)
Few quantitative studies have analyzed the ultrastructure of the human choriocapillaris (CC) and compared the structural variations in disease states to that of age matched controls. This study concentrates on the CC endothelial (EC) cell differences.
Thirty donor eyes (74±7yrs) were obtained from Dr. G. Hageman (Moran Eye Institute, UT) and from Dr. R. Green’s repositories (Wilmer, MD). One eye of each donor was prepared for electron microscopy (TEM). TEM images of the choroidal capillaries (CC) were taken at 4K and 25K. The length of Bruchs membrane (BM) and area of EC soma were measured as well as the area of caveolae and transcytotic vesicles within the EC body. Fenestrations per millimeter of BM were counted. Collages were prepared with a minimum of 3 capillaries of the 25K images for each subject and analyzed with Image J. Patients were divided into five groups: controls (n=6), no chromosomal disorder with no history of AMD; chromosome1-directed AMD (n=4) and chromosome10-directed (n=4); neovascular (NV) AMD(n=8); and geographic atrophy (GA) (n=6). The NV and GA groups were subdivided into border regions in which images were taken adjacent to choroidal neovascularization (CNV) and within or just outside of the atrophic regions in GA.
Based on the Wilcoxon test, significant decreases were found in the number of fenestrations counted from areas under CNV (P=0.039) and in atrophic areas of GA eyes (P=0.020). A significant decrease (P=0.039) was found in the percent of caveole area within the EC bodies of CC beneath CNV. Loss of CC vessels was evident in areas of atrophy and CNV. Capillaries in areas bordering CNV did not have significant loss of fenestrations but appeared to have a slightly increased EC area and with a larger area of caveolae compared to controls. In CC regions of controls and in border areas less affected by disease, fenestrations were observed on both the BM and scleral sides of vessels. CC EC’s in patients with chromosomal disorders exhibited degenerative changes. CC loss was evident in areas of GA and CNV.
CC EC’s show significant changes in the localized areas of pathology in CNV and GA. Subjects with chromosome1 and 10 directed AMD demonstrate marked CC changes and EC degradation. We conclude that CC EC transport systems are severely affected by AMD.
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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