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E-selectin expression on human brain microvascular endothelial cells

D C Hess1, Y Thompson, A Sprinkle

  • 1Neurology Service (127), V.A. Medical Center, Augusta, GA, USA.

Neuroscience Letters
|July 26, 1996
PubMed
Summary
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E-selectin expression in brain endothelial cells is induced by inflammatory stimuli. N-acetylcysteine and dexamethasone inhibit this expression, suggesting a role in mitigating brain inflammation.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • E-selectin is an endothelial adhesion molecule crucial for neutrophil binding and targeting.
  • Its expression and role within the brain microvasculature remain largely uncharacterized.

Purpose of the Study:

  • To investigate the expression of E-selectin on human brain microvascular endothelial cells (HBMEC).
  • To explore the modulatory effects of specific compounds on E-selectin expression and related inflammatory pathways in HBMEC.

Main Methods:

  • Cultured HBMEC were stimulated with inflammatory cytokines (IL-1b, TNF) and lipopolysaccharide (LPS).
  • E-selectin surface expression was quantified using flow cytometry.
  • The impact of N-acetylcysteine (NAC), dimethylthiourea (DMTU), dexamethasone, and allopurinol on E-selectin expression was assessed.

Related Experiment Videos

  • Nuclear factor kappa B (NF-κB) activation by TNF was measured in HBMEC.
  • Main Results:

    • Basal E-selectin expression was absent in HBMEC but induced by IL-1b, TNF, or LPS stimulation within 4 hours.
    • Induced E-selectin expression on HBMEC was quantitatively lower compared to human umbilical vein endothelial cells (HUVEC).
    • N-acetylcysteine (NAC), dimethylthiourea (DMTU), and dexamethasone partially inhibited cytokine-induced E-selectin upregulation.
    • TNF-induced NF-κB activation in HBMEC was attenuated by NAC and dexamethasone treatment.

    Conclusions:

    • E-selectin is expressed on brain microvascular endothelial cells upon inflammatory stimulation.
    • Thiol donors (like NAC) and corticosteroids (like dexamethasone) can inhibit E-selectin expression and NF-κB activation.
    • These findings suggest a potential therapeutic role for thiol donors and corticosteroids in managing neuroinflammatory conditions by modulating neutrophil-endothelial interactions.