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

Abstract : 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 patho-Iogical 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 transendothelial 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 intracellutar 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.
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Journal of Neuroscience Research, Wiley, 1995, 41, p. 717-726
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Soumis le : mercredi 3 novembre 2010 - 14:43:11
Dernière modification le : mercredi 3 novembre 2010 - 14:43:11

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Maria A. Deli, L. Descamps, Marie-Pierre Dehouck, Roméo Cecchelli, Ferenc Joo, et al.. 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. Journal of Neuroscience Research, Wiley, 1995, 41, p. 717-726. 〈hal-00531671〉

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