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Abstract #76905 Published in IGR 19-3
Endothelial Cell Reaction to Elevated Hydrostatic Pressure and Oxidative Stress in Vitro
Mann C; Thanos S; Brockhaus K; Grus FH; Pfeiffer N; Prokosch VKlinische Monatsblätter für Augenheilkunde 2019; 236: 1122-1128
INTRODUCTION: Endothelial dysfunction has become a strongly discussed factor regarding glaucoma pathogenesis. In addition to peripapillary bleedings as signs of vascular damage, there is a definite correlation between glaucoma and vascular dysregulation syndrome. The aim of this study was to evaluate endothelial cell reaction to moderately elevated hydrostatic pressure and oxidative stress in vitro. METHODS: In vitro, primarily dissociated brain microvascular endothelial cells (BMECs) were exposed to moderately elevated hydrostatic pressure (60 and 120 mmHg) in a special pressure chamber. Additionally, cells primarily exposed to pressure, and cells not exposed to pressure, were incubated with low amounts of HO. A live/dead assay was performed to evaluate cell viability. Immunohistochemical staining against actin was used for morphological evaluation. RESULTS: Neither 60 nor 120 mmHg of elevated pressure had a viability changing effect on primary endothelial cells. Secondary, no big morphological changes could be discovered. However, against a low concentration of oxidative stress, BMECs showed high vulnerability. A difference in reaction to cells stressed with high pressure before could not be shown. CONCLUSION: Direct effects, in terms of higher vulnerability or morphological changes of moderately elevated high pressure on endothelial cells, could not be shown. However, the reaction to low amounts of oxidative stress indicates the involvement of endothelial cells in the pathogenesis of glaucoma and the special role of oxidative stress when referring to endothelial dysfunction in glaucomatous disease.
Universitäts-Augenklinik, Universitätsmedizin der Johannes Gutenberg-Universität Mainz.
Full articleClassification:
3.6 Cellular biology (Part of: 3 Laboratory methods)
1.3 Pathogenesis (Part of: 1 General aspects)
