<p>A: Effect on TER of the primary RPMVEC monolayer. Compared with controls, TER of primary RPMVEC monolayer challenged with TNF-α for 2 hours decreased significantly. Pretreatment of the primary RPMVEC with O-Me-cAMP (1 hour) significantly augmented TER and prevented TNF-α-induced the drop of TER. B: Effect on flux of FITC-BSA across the primary RPMVEC monolayer. Compared with untreated cells, the RPMVECs treated with TNF-α for 2 h had higher levels of FITC-BSA flux, whereas O-Me-cAMP treatment alone resulted in decrease FITC-BSA flux. Co-treatment with O-Me-cAMP and TNF-α [i.e., O-Me-cAMP +TNF-α] did not lead to increased endothelial permeability. Each bar represents mean ±SD of four independent trials; * denote <i>P</i><0.05, ** denote <...
<p>A) Analysis of the effects of TNF on actin/CL5 co-localization. Post-confluent HDMEC monolayers i...
<p> Cells were treated with TNF-α (B) for 2 hours or with O-Me-cAMP (C) for 1 hour or co-treated wit...
<p>A: Concentration-dependent inhibition of induction of ICAM-1 expression by IκK-β-inhibitor Bay11,...
<p><i>A</i>. Treatment with the selective Rac1 inhibitor Z62954982 reduces TER in a concentration-de...
<p>A: Effect on TER of PMVEC monolayer. Compared with control shRNA group, the mean baseline TER of ...
<p><i>A</i>. Time course of TER of HUVEC monolayers transfected with WT and DN Rac1 plasmids, treate...
<p><i>A</i>. Rac1-GTP levels in control HUVEC and cells treated with 50 μM NSC23766 for 30 min. <i>B...
<p>(A) For the Dextran assay, cells were cultured in inserts for 24 h followed by applying fluoresce...
<p>(A, B, C) Endothelial cells grown in 24-well plates were treated with vehicle (A, B) or 100 nM Ma...
The endothelium controls the influx of macromolecules into the tissues, a process that may be distur...
<p>(A) Cells were evenly seeded in 96-well plates at a density of 10<sup>3</sup>–10<sup>4</sup> cell...
<p>A. Time course of changes in TER of HUVEC monolayers before and after treatment with 2 μM S1P or ...
<p>(<b>A</b>) Confluent cells were treated with TNF-α (top) or IL-6 (bottom) (0–100 ng/ml, 18 hrs). ...
<p>(A) Confluent HUVEC monolayers were pre-treated with/without G-1 (1 µM) for 45 minutes prior to 1...
<p>Cytoskeletal organization and Rac1 activity in endothelial monolayers is altered by simvastatin t...
<p>A) Analysis of the effects of TNF on actin/CL5 co-localization. Post-confluent HDMEC monolayers i...
<p> Cells were treated with TNF-α (B) for 2 hours or with O-Me-cAMP (C) for 1 hour or co-treated wit...
<p>A: Concentration-dependent inhibition of induction of ICAM-1 expression by IκK-β-inhibitor Bay11,...
<p><i>A</i>. Treatment with the selective Rac1 inhibitor Z62954982 reduces TER in a concentration-de...
<p>A: Effect on TER of PMVEC monolayer. Compared with control shRNA group, the mean baseline TER of ...
<p><i>A</i>. Time course of TER of HUVEC monolayers transfected with WT and DN Rac1 plasmids, treate...
<p><i>A</i>. Rac1-GTP levels in control HUVEC and cells treated with 50 μM NSC23766 for 30 min. <i>B...
<p>(A) For the Dextran assay, cells were cultured in inserts for 24 h followed by applying fluoresce...
<p>(A, B, C) Endothelial cells grown in 24-well plates were treated with vehicle (A, B) or 100 nM Ma...
The endothelium controls the influx of macromolecules into the tissues, a process that may be distur...
<p>(A) Cells were evenly seeded in 96-well plates at a density of 10<sup>3</sup>–10<sup>4</sup> cell...
<p>A. Time course of changes in TER of HUVEC monolayers before and after treatment with 2 μM S1P or ...
<p>(<b>A</b>) Confluent cells were treated with TNF-α (top) or IL-6 (bottom) (0–100 ng/ml, 18 hrs). ...
<p>(A) Confluent HUVEC monolayers were pre-treated with/without G-1 (1 µM) for 45 minutes prior to 1...
<p>Cytoskeletal organization and Rac1 activity in endothelial monolayers is altered by simvastatin t...
<p>A) Analysis of the effects of TNF on actin/CL5 co-localization. Post-confluent HDMEC monolayers i...
<p> Cells were treated with TNF-α (B) for 2 hours or with O-Me-cAMP (C) for 1 hour or co-treated wit...
<p>A: Concentration-dependent inhibition of induction of ICAM-1 expression by IκK-β-inhibitor Bay11,...