June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
A potential neuroprotective role for meningothelial cells
Author Affiliations & Notes
  • Albert Neutzner
    Department Biomedicine, University Hospital Basel, Basel, Switzerland
  • Charles Hemion
    Department Biomedicine, University Hospital Basel, Basel, Switzerland
  • Emilia Meyer
    Department Biomedicine, University Hospital Basel, Basel, Switzerland
  • Corina Kohler
    Department Biomedicine, University Hospital Basel, Basel, Switzerland
  • Hendrik P Scholl
    University Hospital Basel, Basel, Switzerland
  • Peter Meyer
    University Hospital Basel, Basel, Switzerland
  • Hanspeter E. Killer
    Kantonsspital Aarau, Aarau, Switzerland
  • Footnotes
    Commercial Relationships   Albert Neutzner, None; Charles Hemion, None; Emilia Meyer, None; Corina Kohler, None; Hendrik Scholl, None; Peter Meyer, None; Hanspeter Killer, None
  • Footnotes
    Support  Forschungsfond Aarau, Cantonal Hospital Aarau, Switzerland
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 1741. doi:
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      Albert Neutzner, Charles Hemion, Emilia Meyer, Corina Kohler, Hendrik P Scholl, Peter Meyer, Hanspeter E. Killer; A potential neuroprotective role for meningothelial cells. Invest. Ophthalmol. Vis. Sci. 2017;58(8):1741.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Altered cerebrospinal fluid (CSF) homeostasis is thought to be the main culprit of visual impairment during optic nerve compartment syndrome likely due to diminished flow and accumulation of harmful substances in the optic nerve microenvironment. Meningothelial cells (MECs) form the cellular component of this environment and are involved in maintaining CSF homeostasis. MECs are highly active facultative phagocytes promoting the clearance of bacteria and apoptotic cell bodies from the CSF. In addition, MECs are actively modulating immunological processes in the brain through the secretion of pro- and anti-inflammatory cytokines. To better understand the connection between MECs and neuronal damage, we studied the clearance of neurotoxic peptides by these cells.

Methods : Primary human MECs were treated with the neurotoxic peptides amyloid-β (Aβ) and α-synuclein and peptide uptake, mitochondrial function and cell death was assessed and compared to neuronal and astrocytic cells. Phosphokinase arrays were used to analyze signaling pathways after stimulation of MECs with Aβ.

Results : We found that MECs ingest Aβ and α-synuclein up to about 10-fold more efficiently compared to neuronal cells via clathrin- and caveolae-mediated endocytosis as well as macropinocytotic processes. While production of reactive oxygen species (ROS) following exposure to Aβ and α-synuclein was similar between MECs and neuronal cells, mitochondrial function in MECs was significantly more resistant to Aβ treatment compared to neuronal cells. Similarly, MECs were significantly less susceptible to Aβ-induced cell death than neuronal cells. Analysis by phosphokinase array revealed that treatment of MECs with Aβ compared to neuronal cells induced cellular signaling potentially connected to increased resistance to neurotoxic peptides.

Conclusions : MECs are a sink for neurotoxic peptides thereby providing an alternative clearance mechanism for such substances. Thus, altered waste clearance from the microenvironment by MECs during optic nerve compartmentalization might contribute to vision loss.

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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