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Arachnoid cell changes following elevated pressure and oxidative stress: new implications for optic nerve degeneration
Author(s) -
NEUTZNER A,
XIN X,
FAN B,
FLAMMER J,
MILLER NR,
KILLER HE,
MEYER P
Publication year - 2010
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2010.2134.x
Subject(s) - optic nerve , oxidative stress , hydrostatic pressure , chemistry , glaucoma , medicine , pathology , ophthalmology , microbiology and biotechnology , endocrinology , biology , physics , thermodynamics
Purpose The study of meningothelial cells (MCs) and their connection to optic nerve function. MCs line the arachnoid layer of the meninges and form a barrier between the CSF and the blood circulation. A previous study revealed a significantly increased proliferation of MCs in the arachnoid surrounding the optic nerve glaucoma patients. Methods To explore a possible role of these cells in the pathogenesis of diseases of the optic nerve, we studied the effect of elevated hydrostatic pressure and oxidative stress on MCs using rotenone to inhibit mitochondrial function and compared them to untreated control cells. Cell viability and proliferation were measured using a MTS‐based assay. As a measure of barrier function, we assessed the endocytotic activity of MCs by fluorescence and confocal microscopy following fluorescent‐latex bead uptake. Results Exposure of MCs to elevated hydrostatic pressure caused significant cellular proliferation and a dramatic decrease in endocytotic activity. Furthermore, mild oxidative stress severely inhibited endocytosis, thus negatively impacting MC barrier function. Conclusion MCs surround the optic nerve, thereby shielding it from but also conditioning the microenvironment of this sensitive area. As elevated pressure and oxidative stress occur in patients with increased intracranial pressure who have papilledema and probably in some cases of normal‐tension glaucoma, these phenomena may impact the function of MCs and thus, contribute to the loss of retinal ganglion cells in the course of these and, perhaps, other optic nerve diseases.

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