Forskolin regulates retinal endothelial cell permeability through TLR4 actions in vitro

2021 ◽  
Author(s):  
Li Liu ◽  
Youde Jiang ◽  
Jena J. Steinle
Keyword(s):  
Endothelial Cell ◽  
Cell Permeability ◽  
Endothelial Cell Permeability ◽  
Retinal Endothelial Cell

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 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

Increased expression and secretion of resistin in epicardial adipose tissue of patients with acute coronary syndrome

2010 ◽  
Vol 298 (3) ◽  
pp. H746-H753 ◽  
Author(s):  
Silvia Langheim ◽  
Lorella Dreas ◽  
Lorenzo Veschini ◽  
Francesco Maisano ◽  
Chiara Foglieni ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Adipose Tissue ◽  
Endothelial Cell ◽  
Protein Secretion ◽  
Epicardial Adipose Tissue ◽  
Cell Permeability ◽  
Coronary Syndrome ◽  
Endothelial Cell Permeability ◽  
Stable Cad

The purpose of this study was to test the hypothesis that specific epicardial adipose tissue (EAT) proinflammatory adipokines might be implicated in acute coronary syndrome (ACS). We compared expression and protein secretion of several EAT adipokines of male ACS with those of matched stable coronary artery disease (CAD) patients and controls with angiographically normal coronary arteries. The effect of supernatant of cultured EAT on endothelial cell permeability in vitro was also evaluated in the three study groups. EAT of ACS patients showed significantly higher gene expression and protein secretion of resistin than patients with stable CAD. Interleukin-6, plasminogen activator inhibitor-1, and monocyte chemoattractant protein-1 genes were also significantly overexpressed in ACS compared with the control group but not when compared with stable CAD. Immunofluorescence of EAT sections revealed a significantly greater number of CD68+ cells in ACS patients than stable CAD and control groups. The permeability of endothelial cells in vitro was significantly increased after exposure to supernatant of cultured EAT from ACS, but not control or stable CAD groups, and this effect was normalized by anti-resistin antiserum. We found that EAT of patients with ACS is characterized by increased expression and secretion of resistin and associated with increased in vitro endothelial cell permeability.

scholarly journals Long noncoding RNA Hotair facilitates retinal endothelial cell dysfunction in diabetic retinopathy

2020 ◽  
Vol 134 (17) ◽  
pp. 2419-2434
Author(s):  
Di Zhao ◽  
Yanyan Zhao ◽  
Jiao Wang ◽  
Lina Wu ◽  
Yanling Liu ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Endothelial Cell ◽  
Transcriptional Activation ◽  
Noncoding Rna ◽  
Retinal Vessel ◽  
Underlying Mechanism ◽  
Cell Permeability ◽  
Retinal Endothelial Cell

Abstract Background: Retinal endothelial cell (REC) dysfunction induced by diabetes mellitus (DM) is an important pathological step of diabetic retinopathy (DR). Long noncoding RNAs (lncRNAs) have emerged as novel modulators in DR. The present study aimed to investigate the role and mechanism of lncRNA Hotair in regulating DM-induced REC dysfunction. Methods: The retinal vascular preparations and immunohistochemical staining assays were conducted to assess the role of Hotair in retinal vessel impairment in vivo. The EdU, transwell, cell permeability, CHIP, luciferase activity, RIP, RNA pull-down, and Co-IP assays were employed to investigate the underlying mechanism of Hotair-mediated REC dysfunction in vitro. Results: Hotair expression was significantly increased in diabetic retinas and high glucose (HG)-stimulated REC. Hotair knockdown inhibited the proliferation, invasion, migration, and permeability of HG-stimulated REC in vitro and reduced the retinal acellular capillaries and vascular leakage in vivo. Mechanistically, Hotair bound to LSD1 to inhibit VE-cadherin transcription by reducing the H3K4me3 level on its promoter and to facilitate transcription factor HIF1α-mediated transcriptional activation of VEGFA. Furthermore, LSD1 mediated the effects of Hotair on REC function under HG condition. Conclusion: The Hotair exerts its role in DR by binding to LSD1, decreasing VE-cadherin transcription, and increasing VEGFA transcription, leading to REC dysfunction. These findings revealed that Hotair is a potential therapeutic target of DR.

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