PMID- 7500373
OWN - NLM
STAT- MEDLINE
DCOM- 19960118
LR  - 20061115
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 41
IP  - 6
DP  - 1995 Aug 15
TI  - Exposure of tumor necrosis factor-alpha 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.
PG  - 717-26
AB  - Tumor necrosis factor-alpha (TNF-alpha), 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-alpha (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-alpha. On 
      the other hand, at 16 hr after the 1-hr challenge with TNF-alpha (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-alpha by a delayed 
      increase of permeability and reorganization of actin filaments.
FAU - Deli, M A
AU  - Deli MA
AD  - Biological Research Center, Hungarian Academy of Sciences, Szeged, Hungary.
FAU - Descamps, L
AU  - Descamps L
FAU - Dehouck, M P
AU  - Dehouck MP
FAU - Cecchelli, R
AU  - Cecchelli R
FAU - Joo, F
AU  - Joo F
FAU - Abraham, C S
AU  - Abraham CS
FAU - Torpier, G
AU  - Torpier G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Actins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 57-50-1 (Sucrose)
SB  - IM
MH  - Actins/*drug effects
MH  - Animals
MH  - Astrocytes/drug effects
MH  - Blood-Brain Barrier
MH  - Brain/*drug effects
MH  - Cattle
MH  - Cells, Cultured
MH  - Endothelium, Vascular/*drug effects
MH  - Membranes/drug effects
MH  - Microscopy, Confocal
MH  - Permeability/*drug effects
MH  - Sucrose/metabolism
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1995/08/15 00:00
MHDA- 1995/08/15 00:01
CRDT- 1995/08/15 00:00
PHST- 1995/08/15 00:00 [pubmed]
PHST- 1995/08/15 00:01 [medline]
PHST- 1995/08/15 00:00 [entrez]
AID - 10.1002/jnr.490410602 [doi]
PST - ppublish
SO  - J Neurosci Res. 1995 Aug 15;41(6):717-26. doi: 10.1002/jnr.490410602.