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Inflammation and dephosphorylation of the tight junction protein occludin in an experimental model of multiple

L Morgan1, B Shah, L E Rivers

  • 1Eisai London Research Laboratories Ltd., University College London, London, UK.

Neuroscience
|June 15, 2007
PubMed

Insights

In experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis (MS), occludin dephosphorylation precedes blood-brain barrier breakdown, suggesting its role in CNS inflammation.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Multiple sclerosis (MS) is a central nervous system (CNS) disease characterized by inflammation, demyelination, and neurodegeneration.
  • Experimental autoimmune encephalomyelitis (EAE) is a widely used animal model to study MS pathogenesis.
  • Understanding the molecular mechanisms underlying blood-brain barrier (BBB) disruption in EAE is crucial for MS research.

Purpose of the Study:

  • To investigate protein changes in the spinal cord during EAE.
  • To elucidate the role of junctional proteins, specifically occludin, in BBB integrity during EAE.
  • To explore the post-translational modifications of occludin in the context of EAE.

Main Methods:

  • Proteomic analysis of lumbar spinal cord extracts from naïve and EAE rats.
  • Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) to assess protein migration.
  • In vitro phosphatase treatment to investigate occludin dephosphorylation.

Main Results:

  • EAE rats exhibited hallmarks of inflammation and BBB breakdown.
  • Occludin showed increased migration on SDS-PAGE in EAE rats, indicative of dephosphorylation.
  • Occludin dephosphorylation occurred concurrently with inflammation onset and preceded BBB permeability changes.

Conclusions:

  • Occludin dephosphorylation is an early event in EAE pathogenesis.
  • These findings suggest occludin is a signaling target in EAE.
  • Occludin dephosphorylation may play a role in regulating BBB response to inflammation in MS.

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