{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T17:36:27Z","timestamp":1791048987624,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2004,10,11]],"date-time":"2004-10-11T00:00:00Z","timestamp":1097452800000},"content-version":"vor","delay-in-days":3345,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[1995,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Tumor necrosis factor\u2010\u03b1 (TNF\u2010\u03b1), 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\u2010brain 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\u2010hr exposure of recombinant human TNF\u2010\u03b1 (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&lt; 0.05) in sucrose permeation at 2\u20134 hr with the highest dose of TNF\u2010\u03b1 On the other hand, at 16 hr after the 1\u2010hr challenge with TNF\u2010\u03b1 (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\u2010actin 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\u2010\u03b1 by a delayed increase of permeability and reorganization of actin filaments. \u00a91995 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.490410602","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T02:13:23Z","timestamp":1104545603000},"page":"717-726","source":"Crossref","is-referenced-by-count":139,"title":["Exposure of tumor necrosis factor\u2010\u03b1 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"],"prefix":"10.1002","volume":"41","author":[{"given":"M. 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