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In Vitro Assays to Assess Blood-brain Barrier Mesh-like Vessel Formation and Disruption
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Amyloid beta toxicity dependent upon endothelial cell state.

Mercedes Balcells1, Joseph S Wallins, Elazer R Edelman

  • 1Harvard-MIT Division of Health Sciences and Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, United States. merche@mit.edu

Neuroscience Letters
|July 8, 2008
PubMed
Summary
This summary is machine-generated.

Cell state significantly impacts amyloid beta (Abeta) toxicity. Subconfluent cells are more vulnerable to Abeta, suggesting cell condition is crucial for understanding Alzheimer's disease (AD) pathology.

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Published on: July 21, 2012

Area of Science:

  • Cell Biology
  • Neuroscience
  • Vascular Biology

Background:

  • Amyloid beta (Abeta) peptides are implicated in Alzheimer's disease (AD) pathogenesis, forming toxic plaques in the brain.
  • Oxidative stress-induced blood-brain barrier degeneration is a proposed mechanism for Abeta42 toxicity, but doesn't explain its absence in healthy tissues.
  • The role of cell state in mediating Abeta toxicity remains underexplored.

Purpose of the Study:

  • To investigate the hypothesis that cell state mediates the toxic effects of amyloid beta (Abeta).
  • To examine the viability and behavior of endothelial cells (EC), vascular smooth muscle cells (SMC), and epithelial cells (EPI) in different states when exposed to Abeta.

Main Methods:

  • Abeta was secreted from transfected Chinese hamster ovary (CHO) cells and applied to aortic EC, SMC, and EPI in varying states (subconfluent vs. confluent).
  • Cell viability, sprouting (EC), inhibition (SMC, EPI), and Abeta production were assessed.
  • The effects of conditioned media from subconfluent EC on confluent EC in the presence of Abeta were also analyzed.

Main Results:

  • Abeta exhibited higher toxicity to all cell types when they were in a subconfluent state.
  • Subconfluent EC showed sprouting, while SMC and EPI were inhibited by Abeta.
  • Confluent EC were resistant to Abeta and suppressed its production; however, factors from subconfluent EC stimulated Abeta production and toxicity in confluent EC.

Conclusions:

  • Cellular state is a critical mediator of Abeta toxicity, with subconfluent or growth states enhancing cytotoxicity.
  • Findings suggest Abeta42 may be more cytotoxic to cells in injured or actively growing states, potentially explaining variable AD pathology.
  • Future research should consider tissue and cell state, alongside Abeta concentration and exposure time, to understand vascular and cerebral toxicity in AD.