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Endothelial-Derived Extracellular Vesicles Induce Cerebrovascular Dysfunction in Inflammation.

David Roig-Carles1, Eduard Willms2, Ruud D Fontijn3

  • 1School of Life, Health and Chemical Sciences, Biomedical Research Network, Open University, Milton Keynes MK7 6AA, UK.

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Inflamed brain endothelial cell-derived small extracellular vesicles (sEVs) disrupt the blood-brain barrier (BBB). These sEVs increase T-cell adhesion by upregulating VCAM1, contributing to neuroinflammation.

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blood–brain barriercell-to-cell communicationexosomesextracellular vesiclesneuroinflammation

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Immunology

Background:

  • Blood-brain barrier (BBB) dysfunction is central to neuroinflammatory disorders.
  • Extracellular vesicles (EVs) mediate cell-to-cell communication, with circulating EVs altered in neurological conditions.
  • The role of brain endothelial cell (BEC)-derived EVs in BBB dysfunction remains unclear.

Purpose of the Study:

  • To investigate whether EVs derived from inflamed BECs contribute to BBB dysfunction.
  • To characterize the effects of these EVs on BBB integrity and leukocyte adhesion.
  • To identify molecular mechanisms underlying EV-mediated cerebrovascular changes.

Main Methods:

  • Human cerebral microvascular cells (hCMEC/D3) were stimulated with TNFα and IFNy.
  • Small EVs (sEVs) were isolated and characterized.
  • Effects on transendothelial electrical resistance (TEER) and T-cell adhesion were assessed.
  • Molecular changes (microRNA-155, VCAM1, ICAM1) were analyzed via RT-qPCR and Western blotting.

Main Results:

  • sEVs from inflamed hCMEC/D3 cells reduced TEER and increased T-cell adhesion to recipient cells.
  • sEV treatment elevated microRNA-155, VCAM1, and ICAM1 levels in hCMEC/D3 cells.
  • Blocking VCAM1, but not ICAM1, inhibited sEV-induced T-cell adhesion.

Conclusions:

  • sEVs derived from inflamed BECs actively promote cerebrovascular dysfunction.
  • VCAM1 is a key mediator of sEV-induced leukocyte adhesion to the brain endothelium.
  • These findings offer new insights into the pathogenesis of neuroinflammatory disorders.