Dexamethasone reverses the effects of high glucose on human retinal endothelial cell permeability and proliferation in vitro

2016 ◽  
Vol 151 ◽  
pp. 75-81 ◽  
Author(s):  
E.A. Stewart ◽  
S. Saker ◽  
W.M. Amoaku
Keyword(s):  
Endothelial Cell ◽  
High Glucose ◽  
Cell Permeability ◽  
Endothelial Cell Permeability ◽  
Retinal Endothelial Cell ◽  
Proliferation In Vitro

Neoplastic and pharmacological influence on the permeability of an in vitro blood-brain barrier

1995 ◽  
Vol 82 (6) ◽  
pp. 1053-1058 ◽  
Author(s):  
Paul A. Grabb ◽  
Mark R. Gilbert
Keyword(s):  
Endothelial Cell ◽  
Rat Brain ◽  
Phospholipase A ◽  
Cell Permeability ◽  
Capillary Endothelium ◽  
Brain Capillary ◽  
Content Type ◽  
Endothelial Cell Permeability ◽  
Fine Print

✓ The authors investigated the effects of glioma cells and pharmacological agents on the permeability of an in vitro blood-brain barrier (BBB) to determine the following: 1) whether malignant glia increase endothelial cell permeability; 2) how glucocorticoids affect endothelial cell permeability in the presence and absence of malignant glia; and 3) whether inhibiting phospholipase A2, the enzyme that releases arachidonic acid from membrane phospholipids, would reduce any malignant glioma—induced increase in endothelial cell permeability. Primary cultures of rat brain capillary endothelium were grown on porous membranes; below the membrane, C6, 9L rat glioma, T98G human glioblastoma, or no cells (control) were cocultured. Dexamethasone (0.1 µM), bromophenacyl bromide (1.0 µM), a phospholipase A2 inhibitor, or nothing was added to culture media 72 hours prior to assaying the rat brain capillary endothelium permeability. Permeability was measured as the flux of radiolabeled sucrose across the rat brain capillary endothelium monolayer and then calculated as an effective permeability coefficient (Pe). When neither dexamethasone nor bromophenacyl bromide was present, C6 cells reduced the Pe significantly (p < 0.05), whereas 9L and T98G cells increased Pe significantly (p < 0.05) relative to rat brain capillary endothelium only (control). Dexamethasone reduced Pe significantly for all cell preparations (p < 0.05). The 9L and T98G cell preparations coincubated with dexamethasone had the lowest Pe of all cell preparations. The Pe was not affected in any cell preparation by coincubation with bromophenacyl bromide (p > 0.45). These in vitro BBB experiments showed that: 1) malignant glia, such as 9L and T98G cells, increase Pe whereas C6 cells probably provide an astrocytic influence by reducing Pe; 2) dexamethasone provided significant BBB “tightening” effects both in the presence and absence of glioma cells; 3) the in vivo BBB is actively made more permeable by malignant glia and not simply because of a lack of astrocytic induction; 4) tumor or endothelial phospholipase A2 activity is probably not responsible for glioma-induced increased in BBB permeability; and 5) this model is useful for testing potential agents for BBB protection and for studying the pathophysiology of tumor-induced BBB disruption.

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.

scholarly journals High glucose promotes retinal endothelial cell migration through activation of Src, PI3K/Akt1/eNOS, and ERKs

2008 ◽  
Vol 295 (6) ◽  
pp. C1647-C1657 ◽  
Author(s):  
Qiong Huang ◽  
Nader Sheibani
Keyword(s):  
Diabetic Retinopathy ◽  
Endothelial Cell ◽  
Signaling Pathways ◽  
High Glucose ◽  
Vascular Function ◽  
Endothelial Cell Migration ◽  
Retinal Endothelial Cell ◽  
The Impact ◽  
Sustained Activation

Hyperglycemia impacts retinal vascular function and promotes the development and progression of diabetic retinopathy, which ultimately results in growth of new blood vessels and loss of vision. How high glucose affects retinal endothelial cell (EC) properties requires further investigation. Here we determined the impact of high glucose on mouse retinal EC function in vitro. High glucose significantly enhanced the migration of retinal EC without impacting their proliferation, apoptosis, adhesion, and capillary morphogenesis. The enhanced migration of retinal EC under high glucose was reversed in the presence of the antioxidant N-acetylcysteine, suggesting increased oxidative stress under high-glucose conditions. Retinal EC under high-glucose conditions also expressed increased levels of fibronectin, osteopontin, and αvβ3-integrin, and reduced levels of thrombospondin-1. These changes were concomitant with sustained activation of the downstream prosurvival and promigratory signaling pathways, including Src kinase, phosphatidylinositol 3-kinase/Akt1/endothelial nitric oxide synthase, and ERKs. The sustained activation of these signaling pathways was essential for enhanced migration of retinal EC under high-glucose conditions. Together, our results indicate the exposure of retinal EC to high glucose promotes a promigratory phenotype. Thus alterations in the proangiogenic properties of retinal EC during diabetes may contribute to the development and pathogenesis of diabetic retinopathy.

scholarly journals TNF-  Signals Through PKC /NF- B to Alter the Tight Junction Complex and Increase Retinal Endothelial Cell Permeability

Diabetes ◽  
2010 ◽  
Vol 59 (11) ◽  
pp. 2872-2882 ◽  
Author(s):  
C. A. Aveleira ◽  
C.-M. Lin ◽  
S. F. Abcouwer ◽  
A. F. Ambrosio ◽  
D. A. Antonetti
Keyword(s):  
Endothelial Cell ◽  
Tight Junction ◽  
Cell Permeability ◽  
Tight Junction Complex ◽  
Endothelial Cell Permeability ◽  
Retinal Endothelial Cell
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