Vascular Endothelial Growth Factor Fails to Acutely Modulate Endothelial Permeability during Early Angiogenesis in the Chick Chorioallantoic Membrane

2000 ◽  
Vol 60 (3) ◽  
pp. 212-221 ◽  
Author(s):  
Lisa M. DeFouw ◽  
David O. DeFouw
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Chorioallantoic Membrane ◽  
Endothelial Permeability ◽  
Vascular Endothelial ◽  
Chick Chorioallantoic Membrane ◽  
Endothelial Growth Factor

Moderate levels of ethanol induce expression of vascular endothelial growth factor and stimulate angiogenesis

2001 ◽  
Vol 281 (1) ◽  
pp. R365-R372 ◽  
Author(s):  
Jian-Wei Gu ◽  
Jesse Elam ◽  
Amanda Sartin ◽  
Wen Li ◽  
Raymond Roach ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Negative Impact ◽  
Chorioallantoic Membrane ◽  
Epidemiological Studies ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Vegf Mrna ◽  
Chick Chorioallantoic Membrane ◽  
Endothelial Growth Factor

Alcohol abuse has a negative impact on human health; however, epidemiological studies show that moderate consumption of ethanol (EtOH) reduces the risk of coronary heart disease, sudden cardiac death, and ischemic stroke. The mechanisms for these reductions in cardiovascular disease are not well established. Using cultured coronary artery vascular smooth muscle cells, we found that moderate levels of EtOH (10 and 20 mM) caused dose-related increases in both vascular endothelial growth factor (VEGF) mRNA (Northern blot) expression (1.9- and 2.6-fold) and VEGF protein (ELISA) expression (19 and 68%) compared with control ( P < 0.05). EtOH at 0.25 g · kg−1 · day−1 (7 days) increased VEGF mRNA expression by 1.48-fold over control, and increased vessel length density from 3.9 ± 0.7 (control) to 6.0 ± 0.3 mm/mm2 ( P < 0.05) in chick chorioallantoic membrane (CAM). We conclude that moderate levels of ethanol can induce VEGF expression and stimulate angiogenesis in chick CAM. Therefore, the results provide a theoretical basis for speculating that the cardiovascular-protective effects of moderate alcohol consumption may be partly mediated through VEGF-induced angiogenesis.

In vitro release of vascular endothelial growth factor during platelet aggregation

1998 ◽  
Vol 275 (3) ◽  
pp. H1054-H1061 ◽  
Author(s):  
James P. Maloney ◽  
Christopher C. Silliman ◽  
Daniel R. Ambruso ◽  
Jun Wang ◽  
Rubin M. Tuder ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Platelet Aggregation ◽  
Growth Factor ◽  
Platelet Rich Plasma ◽  
In Vitro Release ◽  
Endothelial Permeability ◽  
Vascular Endothelial ◽  
Vessel Injury ◽  
Endothelial Growth Factor

Platelet aggregation is a cardinal feature of both vascular repair and vascular disease. During aggregation platelets release a variety of vasoactive substances; some of these promote angiogenesis, endothelial permeability, and endothelial growth, actions shared by vascular endothelial growth factor (VEGF). This study was undertaken to investigate the hypothesis that VEGF is released by aggregating platelets. We found that VEGF was secreted during the in vitro aggregation of platelet-rich plasma induced by thrombin, collagen, epinephrine, and ADP (range 23–518 pg VEGF/ml). Furthermore, serum VEGF levels were elevated compared with plasma (230 ± 63 vs. 38 ± 8 pg VEGF/ml), indicative of VEGF release during whole blood coagulation. Lysates of apheresed, leukocyte-poor platelet units contained significant amounts of VEGF (2.4 ± 0.8 pg VEGF/mg protein). VEGF message and protein were also present in a megakaryocytic cell line (Dami cell). These results suggest constitutive roles for platelet VEGF in the repair of intimal vessel injury and in the altered permeability and intimal proliferation seen at sites of platelet aggregation and thrombosis.

scholarly journals Streptococcus pneumoniae Induces Secretion of Vascular Endothelial Growth Factor by Human Neutrophils

2000 ◽  
Vol 68 (8) ◽  
pp. 4792-4794 ◽  
Author(s):  
Michiel van der Flier ◽  
Frank Coenjaerts ◽  
Jan L. L. Kimpen ◽  
Andy M. Hoepelman ◽  
Sibyl P. M. Geelen
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Vascular Permeability ◽  
Pneumococcal Disease ◽  
Endothelial Permeability ◽  
Human Neutrophils ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
Stimulation Of

ABSTRACT Infection by pneumococci causes an acute inflammatory response associated with neutrophil influx, increased vascular permeability, and edema. Vascular endothelial growth factor (VEGF) is one of the most potent regulators of endothelial permeability. In vitro stimulation of neutrophils showed that pneumococci and purified pneumococcal cell wall induce VEGF secretion, independent of the presence of pneumolysin or polysaccharide capsule. The results of this study indicate VEGF is secreted in pneumococcal disease, suggesting a role as a mediator of increased vascular permeability.

scholarly journals Transactivation of Vascular Endothelial Growth Factor Receptor-2 by Interleukin-8 (IL-8/CXCL8) Is Required for IL-8/CXCL8-induced Endothelial Permeability

2007 ◽  
Vol 18 (12) ◽  
pp. 5014-5023 ◽  
Author(s):  
Melissa L. Petreaca ◽  
Min Yao ◽  
Yan Liu ◽  
Kathryn DeFea ◽  
Manuela Martins-Green
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Complex Formation ◽  
Growth Factor Receptor ◽  
Endothelial Permeability ◽  
Interleukin 8 ◽  
Src Kinases ◽  
Vascular Endothelial ◽  
Receptor Complex ◽  
Endothelial Growth Factor

Interleukin-8 (IL-8/CXCL8) is a chemokine that increases endothelial permeability during early stages of angiogenesis. However, the mechanisms involved in IL-8/CXCL8-induced permeability are poorly understood. Here, we show that permeability induced by this chemokine requires the activation of vascular endothelial growth factor receptor-2 (VEGFR2/fetal liver kinase 1/KDR). IL-8/CXCL8 stimulates VEGFR2 phosphorylation in a VEGF-independent manner, suggesting VEGFR2 transactivation. We investigated the possible contribution of physical interactions between VEGFR2 and the IL-8/CXCL8 receptors leading to VEGFR2 transactivation. Both IL-8 receptors interact with VEGFR2 after IL-8/CXCL8 treatment, and the time course of complex formation is comparable with that of VEGFR2 phosphorylation. Src kinases are involved upstream of receptor complex formation and VEGFR2 transactivation during IL-8/CXCL8-induced permeability. An inhibitor of Src kinases blocked IL-8/CXCL8-induced VEGFR2 phosphorylation, receptor complex formation, and endothelial permeability. Furthermore, inhibition of the VEGFR abolishes RhoA activation by IL-8/CXCL8, and gap formation, suggesting a mechanism whereby VEGFR2 transactivation mediates IL-8/CXCL8-induced permeability. This study points to VEGFR2 transactivation as an important signaling pathway used by chemokines such as IL-8/CXCL8, and it may lead to the development of new therapies that can be used in conditions involving increases in endothelial permeability or angiogenesis, particularly in pathological situations associated with both IL-8/CXCL8 and VEGF.

scholarly journals The effect of methenamine on vascular development: Experimental investigation using in vivo and insilico methods

2020 ◽  
Author(s):  
Hadi Tavakkoli ◽  
Masoud Imani ◽  
Seyyed Mohammad Rahchamani ◽  
Mohsen Rezvani
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Vascular Development ◽  
Chorioallantoic Membrane ◽  
Treated Group ◽  
Inhibitory Effect ◽  
Control Group ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Background: Methenamine is a worldwide antibacterial agent for urinary system infections in human and animals. The effect of methenamine consumption during early phase of pregnancy is not fully clarified in previous studies. Vascular development is the essential part of the early embryonic growth. Objective: In this study, we used chicken chorioallantoic membrane to evaluate the effects of methenamine administration on angiogenesis process as a model. Materials and Methods: In this experimental study, 20 Ross 308 eggs (mean weight 55 ± 4) were incubated. The eggs were divided into two equal groups (n = 10/each). In the first group, methenamine (150 mg/kg egg weight) was injected on the shell membrane, and in the second group (control group) phosphate-buffered saline as injected. Methenamine was inoculated at 96 and 120 hr after incubation; 24 hr after the last inoculation, the eggs were removed and the egg’s shell was incised. Then, the development of vascular network and vascular endothelial growth factor A expression was evaluated. Results: Angiogenesis was significantly decreased after methenamine treatment. The indexes such as areas containing vessels, the vessels’ length, the percentage of angiogenesis developing areas, and vascular complexity in the treatment group receiving methenamine were significantly reduced compared to the control group. Vascular endothelial growth factor A expression was suppressed in the methenamine treated group. Conclusion: According to the achieved results, it was defined that methenamine could have an inhibitory effect on the growth and development procedures of extraembryonic vasculature. Key words: Methenamine, Angiogenesis modulating agents, Vascular endothelial growth factor A, Extraembryonic membranes.

Diverse effects of vascular endothelial growth factor on human pulmonary endothelial barrier and migration

2006 ◽  
Vol 291 (4) ◽  
pp. L718-L724 ◽  
Author(s):  
T. Mirzapoiazova ◽  
I. Kolosova ◽  
P. V. Usatyuk ◽  
V. Natarajan ◽  
A. D. Verin
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Endothelial Permeability ◽  
Barrier Properties ◽  
Cellular Migration ◽  
Endothelial Barrier ◽  
Intracellular Camp ◽  
Vascular Endothelial ◽  
Pulmonary Endothelium ◽  
Endothelial Growth Factor

Increased endothelial permeability is involved in the pathogenesis of many cardiovascular and pulmonary diseases. Vascular endothelial growth factor (VEGF) is a permeability-increasing cytokine. At the same time, VEGF is known to have a beneficial effect on endothelial cells (EC), increasing their survival. Pulmonary endothelium, particularly, may be exposed to higher VEGF concentrations, since the VEGF level is the higher in the lungs than in any other organ. The purpose of this work was to evaluate the effects of VEGF on barrier function and motility of cultured human pulmonary EC. Using transendothelial resistance measurements as an indicator of permeability, we found that 10 ng/ml VEGF significantly improved barrier properties of cultured human pulmonary artery EC (118.6 ± 0.6% compared with 100% control, P < 0.001). In contrast, challenge with 100 ng/ml VEGF decreased endothelial barrier (71.6 ± 1.0% compared with 100% control, P < 0.001) and caused disruption of adherens junctions. VEGF at both concentrations increased cellular migration; however, 10 ng/ml VEGF had a significantly stronger effect. VEGF caused a dose-dependent increase in intracellular Ca2+ concentration; however, phosphorylation of myosin light chain was detectably elevated only after treatment with 100 ng/ml. In contrast, 10 ng/ml but not 100 ng/ml VEGF caused a significant increase in intracellular cAMP (known barrier-protective stimulus) compared with nonstimulated cells (1,096 ± 157 and 610 ± 86 fmol/mg, respectively; P < 0.024). Y576-specific phosphorylation of focal adhesion kinase was also stimulated by 10 ng/ml VEGF. Our data suggest that, depending on its concentration, VEGF may cause diverse effects on pulmonary endothelial permeability via different signaling pathways.

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