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The Blood-brain Barrier00:49

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Intrinsic blood-brain barrier dysfunction contributes to multiple sclerosis pathogenesis.

Hideaki Nishihara1, Sylvain Perriot2, Benjamin D Gastfriend3

  • 1Theodor Kocher Institute, University of Bern, 3012 Bern, Switzerland.

Brain : a Journal of Neurology
|January 27, 2022
PubMed
Summary

Multiple sclerosis (MS) involves intrinsic blood-brain barrier (BBB) defects, not just neuroinflammation. Human stem cell models reveal MS-derived BBB cells have impaired function and increased inflammation, offering new therapeutic targets.

Keywords:
blood–brain barrierhuman induced pluripotent stem cellsimmune cell migrationmultiple sclerosispermeability

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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Blood-brain barrier (BBB) breakdown and immune cell infiltration into the central nervous system (CNS) are key features of multiple sclerosis (MS).
  • Current understanding suggests BBB dysfunction is primarily a consequence of neuroinflammation, but intrinsic BBB alterations in MS patients remain under investigation.

Purpose of the Study:

  • To investigate whether intrinsic alterations in the BBB of MS patients contribute to MS pathogenesis.
  • To develop and utilize an in vitro model of the BBB using human induced pluripotent stem cells (iPSCs) from MS patients and healthy controls.

Main Methods:

  • Differentiated human iPSCs from MS patients and healthy controls into brain microvascular endothelial cell (BMEC)-like cells to model the BBB.
  • Assessed junctional integrity, barrier properties, efflux pump activity, and inflammatory phenotype (adhesion molecule expression, immune cell interactions) of MS-derived BMEC-like cells.
  • Investigated the effect of Wnt/β-catenin signaling activation on MS-derived endothelial progenitor cells.

Main Results:

  • MS-derived BMEC-like cells exhibited impaired junctional integrity, reduced barrier properties, and decreased efflux pump activity compared to controls.
  • MS-derived BMEC-like cells displayed an inflammatory phenotype, with increased adhesion molecule expression and heightened immune cell interactions.
  • Activation of Wnt/β-catenin signaling improved barrier characteristics and reduced the inflammatory phenotype in MS-derived endothelial progenitor cells.

Conclusions:

  • This study provides evidence for intrinsic BBB impairment in MS patients, which can be effectively modeled using human iPSC-derived BMEC-like cells.
  • Human iPSC-derived BMEC-like cells are a valuable tool for exploring the molecular mechanisms of BBB dysfunction in MS.
  • These findings suggest potential novel therapeutic targets for stabilizing the BBB in multiple sclerosis.