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Exposure of tumor necrosis factor‐α to luminal membrane of bovine brain capillary endothelial cells cocultured with astrocytes induces a delayed increase of permeability and cytoplasmic stress fiber formation of actin
Author(s) -
Deli M. A.,
Descamps L.,
Dehouck M.P.,
Cecchelli R.,
Joó F.,
Ábrahám C. S.,
Torpier G.
Publication year - 1995
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490410602
Subject(s) - tumor necrosis factor alpha , blood–brain barrier , proinflammatory cytokine , cytokine , vascular permeability , chemistry , stress fiber , microbiology and biotechnology , biology , biophysics , endocrinology , medicine , immunology , central nervous system , inflammation , cytoskeleton , biochemistry , cell
Tumor necrosis factor‐α (TNF‐α), a proinflammatory cytokine, has long been known to be involved in the pathogenesis of central nervous system infections and of certain neurodegenerative diseases. However, the possible role of the blood‐brain barrier (BBB), the active interface between the blood circulation and brain tissue, remained unknown during these pathological conditions. In our in vitro reconstructed BBB model, 1‐hr exposure of recombinant human TNF‐α (in concentrations of 50, 250, and 500 U/ml, respectively) to the luminal membrane of bovine brain capillary endothelial cells (BBCEC) did not change significantly the transendothelia: flux of either sucrose (m.w. 342 Da), or inulin (m.w. 5 kDa) up to 4 hr (early phase), except for a slight decrease (P< 0.05) in sucrose permeation at 2–4 hr with the highest dose of TNF‐α On the other hand, at 16 hr after the 1‐hr challenge with TNF‐α (delayed phase) at all 3 concentrations, significant increase was induced in the permeability of BBCEC monolayers for both markers. These changes of permeability were accompanied by a selective reorganization of F‐actin filaments into stress fibers, while the intracellular distribution of vimentin remained similar to the control. These results suggest that BBCEC can respond directly to TNF‐α by a delayed increase of permeability and reorganization of actin filaments. ©1995 Wiley‐Liss, Inc.