scholarly journals EPAC1 controls vascular endothelial cell permeability and the adaptation of these cells to differential fluid shear stress

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Sarah N Rampersad ◽  
Milosz Kaczmarek ◽  
Donald H Maurice
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Fluid Shear Stress ◽  
Vascular Endothelial Cell ◽  
Cell Permeability ◽  
Vascular Endothelial ◽  
Fluid Shear ◽  
Endothelial Cell Permeability

scholarly journals Turbulent fluid shear stress induces vascular endothelial cell turnover in vitro.

1986 ◽  
Vol 83 (7) ◽  
pp. 2114-2117 ◽  
Author(s):  
P. F. Davies ◽  
A. Remuzzi ◽  
E. J. Gordon ◽  
C. F. Dewey ◽  
M. A. Gimbrone
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Fluid Shear Stress ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Cell Turnover ◽  
Fluid Shear ◽  
Turbulent Fluid

scholarly journals cAMP‐signaling via EPAC1 mediates vascular endothelial cell adaptation to fluid‐shear stress

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Sarah Rampersad ◽  
Fabien Hubert ◽  
Maria Umana ◽  
Silja Freitag ◽  
Nathalie Butler ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Fluid Shear Stress ◽  
Vascular Endothelial Cell ◽  
Camp Signaling ◽  
Vascular Endothelial ◽  
Fluid Shear ◽  
Cell Adaptation

scholarly journals Diesel exhaust particles modulate vascular endothelial cell permeability: Implication of ZO-1 expression

2010 ◽  
Vol 197 (3) ◽  
pp. 163-168 ◽  
Author(s):  
Rongsong Li ◽  
Zhi Ning ◽  
Jeffrey Cui ◽  
Fei Yu ◽  
Constantinos Sioutas ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Diesel Exhaust ◽  
Vascular Endothelial Cell ◽  
Diesel Exhaust Particles ◽  
Cell Permeability ◽  
Vascular Endothelial ◽  
Endothelial Cell Permeability ◽  
Exhaust Particles

TOMOR NECROSIS FACTOR AND INTERLEUKIN 1-α INCREASE VASCULAR ENDOTHELIAL CELL PERMEABILITY

1988 ◽  
Vol 16 (4) ◽  
pp. 396
Author(s):  
James A Royall ◽  
Roger L Berkow ◽  
Joseph S Beckman ◽  
Bruce A Freeman
Keyword(s):  
Endothelial Cell ◽  
Interleukin 1 ◽  
Vascular Endothelial Cell ◽  
Cell Permeability ◽  
Vascular Endothelial ◽  
Endothelial Cell Permeability ◽  
Necrosis Factor

Tumor necrosis factor and interleukin 1 alpha increase vascular endothelial permeability

1989 ◽  
Vol 257 (6) ◽  
pp. L399-L410 ◽  
Author(s):  
J. A. Royall ◽  
R. L. Berkow ◽  
J. S. Beckman ◽  
M. K. Cunningham ◽  
S. Matalon ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Interleukin 1 ◽  
Endotoxic Shock ◽  
Cell Monolayer ◽  
Vascular Endothelial Cell ◽  
Cell Permeability ◽  
Vascular Endothelial ◽  
Endothelial Cell Permeability ◽  
Necrosis Factor

Endotoxic shock is associated with acute vascular endothelial injury resulting in edema. Tumor necrosis factor (TNF) and interleukin 1 (IL-1) are cytokines produced by endotoxin-stimulated mononuclear phagocytes that are potential mediators of endotoxic shock. In this study, we investigated the effects of TNF and IL-1 alpha on vascular endothelial cell permeability in vitro. The movement of radiolabeled macromolecules of different sizes (57Co-vitamin B12, 125I-cytochrome c, and 131I-albumin; 6.5-35A) across bovine aortic endothelial cell monolayers was measured after exposure to these cytokines. TNF induced a time- and dose-dependent increase in endothelial cell monolayer permeability that was enhanced in the presence of serum. The peak increase was noted after 12 h of incubation with less alteration of permeability with longer incubations. IL-1 alpha caused a similar time-dependent increase in endothelial cell monolayer permeability, but the peak effect of IL-1 alpha was seen after 24 h. Therefore the increased permeability seen with TNF cannot be explained by release of endogenous IL-1 alone. Neither TNF nor IL-1 alpha increased release of [14C]adenine, and the only effect on lactate dehydrogenase release was a small, but statistically significant, increase after 24 h of incubation. From these studies, we conclude that TNF and IL-1 alpha directly increase vascular endothelial cell permeability in vitro and speculate that these cytokines may be involved in the acute vascular endothelial injury associated with endotoxic shock.

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