Transforming growth factor β1 inhibits cytokine-induced CNS endothelial cell activation

Paula Dore-Duffy*, Roumen Balabanov, Ruth Washington, Robert H. Swanborg

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

Abstract

Postcapillary endothelium at the sites of inflammation undergoes a series of changes collectively termed endothelial cell activation. Activated endothelium expresses immunologically relevant surface proteins that include MHC class II antigens (Ags) and adhesion proteins, as well as exhibits a number of functional changes. Endothelial activation has not been thoroughly studied in CNS endothelium. We have examined cytokine-mediated endothelial activation in isolated rat CNS microvessels. Freshly isolated rat CNS microvessels are viable in culture for at least 72 h. Untreated microvessels express no endothelial activation antigens, but do exhibit constitutive expression of the transferrin receptor (tfR). INFγ induces a dose-dependent increase in both MHC class II antigens and tfR measured by immunofluorescent staining and quantitated by laser cytometry. IFNγ-mediated endothelial cell activation could be inhibited with as little as 2 ng/mL TGF-β1, although 100% inhibition was seen with 10 ng/mL TGF-β1. Cytokinepreactivated endothelial expression of class II Ag and tfR could also be inhibited by TGF-β1. TGF-β1-treated microvessels become anergic to IFNγ stimulation. Results suggest that TGF-β1 may have a regulatory role in endothelial activation.

Original languageEnglish (US)
Pages (from-to)161-175
Number of pages15
JournalMolecular and Chemical Neuropathology
Volume22
Issue number3
DOIs
StatePublished - Aug 1994

Keywords

  • CNS endothelial cells
  • TGF-β
  • adhesion proteins
  • anergy
  • blood-brain barrier
  • capillary
  • cytokines
  • endothelial cell activation
  • inflammation
  • interferon γ
  • laser cytometry
  • transferrin receptors

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology

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