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Loss of CD34 expression in aging human choriocapillaris endothelial cells
Journal article   Open access   Peer reviewed

Loss of CD34 expression in aging human choriocapillaris endothelial cells

Elliott H Sohn, Miles J Flamme-Wiese, S Scott Whitmore, Kai Wang, Budd A Tucker and Robert F Mullins
PloS one, Vol.9(1), pp.e86538-e86538
2014
DOI: 10.1371/journal.pone.0086538
PMCID: PMC3897719
PMID: 24466138
url
https://doi.org/10.1371/journal.pone.0086538View
Published (Version of record) Open Access

Abstract

Structural and gene expression changes in the microvasculature of the human choroid occur during normal aging and age-related macular degeneration (AMD). In this study, we sought to determine the impact of aging and AMD on expression of the endothelial cell glycoprotein CD34. Sections from 58 human donor eyes were categorized as either young (under age 40), age-matched controls (> age 60 without AMD), or AMD affected (>age 60 with early AMD, geographic atrophy, or choroidal neovascularization). Dual labeling of sections with Ulex europaeus agglutinin-I lectin (UEA-I) and CD34 antibodies was performed, and the percentage of capillaries labeled with UEA-I but negative for anti-CD34 was determined. In addition, published databases of mouse and human retinal pigment epithelium-choroid were evaluated and CD34 expression compared between young and old eyes. Immunohistochemical studies revealed that while CD34 and UEA-I were colocalized in young eyes, there was variable loss of CD34 immunoreactivity in older donor eyes. While differences between normal aging and AMD were not significant, the percentage of CD34 negative capillaries in old eyes, compared to young eyes, was highly significant (p = 3.8×10(-6)). Endothelial cells in neovascular membranes were invariably CD34 positive. Published databases show either a significant decrease in Cd34 (mouse) or a trend toward decreased CD34 (human) in aging. These findings suggest that UEA-I and endogenous alkaline phosphatase activity are more consistent markers of aging endothelial cells in the choroid, and suggest a possible mechanism for the increased inflammatory milieu in the aging choroid.
Eye - metabolism Retinal Pigment Epithelium - metabolism Antigens, CD34 - metabolism Choroid - metabolism Endothelial Cells - metabolism Humans Middle Aged Child, Preschool Pigment Epithelium of Eye - metabolism Young Adult Macular Degeneration - metabolism Choroidal Neovascularization - metabolism Cellular Senescence Adolescent Aged, 80 and over Adult Aged Capillaries - metabolism Child Aging - metabolism

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