Proliferation Signal Inhibitor–induced Decrease of Vascular Endothelial Cadherin Expression and Increase of Endothelial Permeability In Vitro Are Prevented by an Anti-oxidant

2008 ◽  
Vol 27 (12) ◽  
pp. 1311-1318 ◽  
Author(s):  
Melinda Oroszlán ◽  
Michael Bieri ◽  
Nathalie Ligeti ◽  
Aniko Farkas ◽  
Simon C. Koestner ◽  
...  
Keyword(s):  
Endothelial Permeability ◽  
Vascular Endothelial ◽  
Vascular Endothelial Cadherin ◽  
Anti Oxidant

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.

Estrogens modulate bovine vascular endothelial cell permeability and HSP 25 expression concomitantly

1998 ◽  
Vol 275 (3) ◽  
pp. H1011-H1015 ◽  
Author(s):  
F. Delarue ◽  
S. Daunes ◽  
R. Elhage ◽  
A. Garcia ◽  
F. Bayard ◽  
...  
Keyword(s):  
Vascular Endothelial Cells ◽  
Low Density Lipoprotein ◽  
Vascular Endothelial Cell ◽  
Density Lipoprotein ◽  
Endothelial Permeability ◽  
Fluid Phase ◽  
Cell Permeability ◽  
Vascular Endothelial ◽  
Macromolecular Transport

The atheroprotective properties of estrogens are supported by clinical data from postmenopausal women who use estrogen replacement therapy. However, the mechanisms mediating activity remain unknown, and it has been suggested that estrogens may help to modulate endothelial permeability to atherogenic lipoproteins. In these studies we used bovine vascular endothelial cells as an in vitro model to show that estrogens were able to regulate low-density lipoprotein transport and permeability of the endothelial monolayer. Macromolecular transport was observed to be a second-order polynomial function of estrogen concentration. Moreover, this regulation was correlated with expression of heat shock protein (HSP) 25, which is known to influence fluid phase pinocytosis and cytoskeleton remodeling, thus suggesting a role for HSP 25 in the estrogenic control of transcellular permeability of the endothelium monolayer.

scholarly journals Role of kinase-independent and -dependent functions of FAK in endothelial cell survival and barrier function during embryonic development

2010 ◽  
Vol 189 (6) ◽  
pp. 955-965 ◽  
Author(s):  
Xiaofeng Zhao ◽  
Xu Peng ◽  
Shaogang Sun ◽  
Ann Y.J. Park ◽  
Jun-Lin Guan
Keyword(s):  
Endothelial Cell ◽  
Normal Development ◽  
Vascular Development ◽  
Vascular Endothelial ◽  
Vascular Endothelial Cadherin ◽  
Abnormal Distribution ◽  
Endothelial Cell Survival ◽  
Independent Functions

Focal adhesion kinase (FAK) is essential for vascular development as endothelial cell (EC)–specific knockout of FAK (conditional FAK knockout [CFKO] mice) leads to embryonic lethality. In this study, we report the differential kinase-independent and -dependent functions of FAK in vascular development by creating and analyzing an EC-specific FAK kinase-defective (KD) mutant knockin (conditional FAK knockin [CFKI]) mouse model. CFKI embryos showed apparently normal development through embryonic day (E) 13.5, whereas the majority of CFKO embryos died at the same stage. Expression of KD FAK reversed increased EC apoptosis observed with FAK deletion in embryos and in vitro through suppression of up-regulated p21. However, vessel dilation and defective angiogenesis of CFKO embryos were not rescued in CFKI embryos. ECs without FAK or expressing KD FAK showed increased permeability, abnormal distribution of vascular endothelial cadherin (VE-cadherin), and reduced VE-cadherin Y658 phosphorylation. Together, our data suggest that kinase-independent functions of FAK can support EC survival in vascular development through E13.5 but are insufficient for maintaining EC function to allow for completion of embryogenesis.

scholarly journals Direct current electric field regulates endothelial permeability under physiologically relevant fluid forces in a microfluidic vessel bifurcation model

Lab on a Chip ◽  
2021 ◽  
Author(s):  
Prashanth Mohana Sundaram ◽  
Kaushik K. Rangharajan ◽  
Ehsan Akbari ◽  
Tanner J. Hadick ◽  
Jonathan W. Song ◽  
...  
Keyword(s):  
Electric Fields ◽  
Tissue Regeneration ◽  
Direct Current ◽  
Endothelial Permeability ◽  
Vascular Endothelial ◽  
Fluid Forces ◽  
Direct Current Electric Field ◽  
On Chip ◽  
Current Electric Field

In vitro model for blood vessel on-chip reporting on the use of direct current electric fields (DC-EFs) to regulate vascular endothelial permeability, which is important for tissue regeneration and wound healing.

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.

Phenotype and hematopoietic potential of side population cells throughout embryonic development

Blood ◽  
2003 ◽  
Vol 102 (7) ◽  
pp. 2436-2443 ◽  
Author(s):  
Brian M. Nadin ◽  
Margaret A. Goodell ◽  
Karen K. Hirschi
Keyword(s):  
Bone Marrow ◽  
Side Population ◽  
Vascular Endothelial ◽  
Hematopoietic Progenitor ◽  
Hematopoietic Stem ◽  
Murine Bone Marrow ◽  
Embryonic Tissues ◽  
Vascular Endothelial Cadherin ◽  
Endothelial Receptor

Abstract Adult murine bone marrow hematopoietic stem cells (HSCs) can be purified by sorting Hoechst 33342-extruding side population (SP) cells. Herein we investigated whether SP cells reside within embryonic tissues and exhibit hematopoietic progenitor activity. We isolated yolk sac (YS) and embryonic tissues 7.5 to 11.5 days after coitus (dpc), resolved an SP in each, and demonstrated that these SP cells exhibit distinct phenotypic and functional characteristics throughout development. YS and embryonic SP isolated 8.0 dpc expressed vascular endothelial-cadherin (VE-cadherin) and vascular endothelial receptor 2 (Flk-1), markers not expressed by bone marrow SP but expressed by endothelial cells and progenitors. SP at this stage did not express CD45 or produce hematopoietic colonies in vitro. In contrast, SP isolated 9.5 to 11.5 dpc contained a significantly higher proportion of cells expressing cKit and CD45, markers highly expressed by bone marrow SP. Furthermore, YS SP isolated 9.5 to 11.5 dpc demonstrated 40- to 90-fold enrichment for hematopoietic progenitor activity over unfractionated tissue. Our data indicate that YS and embryonic SP cells detected prior to the onset of circulation express the highest levels of endothelial markers and do not generate blood cells in vitro; however, as development progresses, they acquire hematopoietic potential and phenotypic characteristics similar to those of bone marrow SP. (Blood. 2003;102:2436-2443)

Correspondence of the Effect of Shear Stress Magnitude on Endothelial Cell Alignment and Heparan Sulfate Expression

2010 ◽  
Author(s):  
Charles S. Wallace ◽  
Tobias Hasenberg ◽  
Morton H. Friedman
Keyword(s):  
Nitric Oxide ◽  
Heparan Sulfate ◽  
Cell Junctions ◽  
Endothelial Glycocalyx ◽  
Vascular Endothelial ◽  
Blood Components ◽  
Cell Alignment ◽  
Vascular Endothelial Cadherin ◽  
Endothelial Functions

The endothelial glycocalyx is believed to play a crucial role in many endothelial functions, including mechanotransduction [1,2], modulation of vascular permeability, and interaction with blood components [3]. A principal constituent of the glycocalyx, thought to sense shearing forces and convey this signal into the cell, is the glycosaminoglycan heparan sulfate (HS). Previous in vitro studies have shown that batch removal of 60% of the heparan sulfate within the glycocalyx inhibits the steady shear-induced production of nitric oxide [4], cell alignment, cell migration, suppression of cell proliferation, and accumulation of vascular endothelial cadherin in cell-cell junctions [5].

scholarly journals Dasatinib increases endothelial permeability leading to pleural effusion

2018 ◽  
Vol 51 (1) ◽  
pp. 1701096 ◽  
Author(s):  
Carole Phan ◽  
Etienne-Marie Jutant ◽  
Ly Tu ◽  
Raphaël Thuillet ◽  
Andrei Seferian ◽  
...  
Keyword(s):  
Pleural Effusion ◽  
Kinase Inhibitor ◽  
Umbilical Vein ◽  
Endothelial Permeability ◽  
Cell Junctions ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Umbilical Vein Endothelial Cells

Pleural effusion is a frequent side-effect of dasatinib, a second-generation tyrosine kinase inhibitor used in the treatment of chronic myelogenous leukaemia. However, the underlying mechanisms remain unknown. We hypothesised that dasatinib alters endothelial integrity, resulting in increased pulmonary vascular endothelial permeability and pleural effusion.To test this, we established the first animal model of dasatinib-related pleural effusion, by treating rats with a daily regimen of high doses of dasatinib (10 mg·kg−1·day−1 for 8 weeks).Pleural ultrasonography revealed that rats chronically treated with dasatinib developed pleural effusion after 5 weeks. Consistent with these in vivo observations, dasatinib led to a rapid and reversible increase in paracellular permeability of human pulmonary endothelial cell monolayers as reflected by increased macromolecule passage, loss of vascular endothelial cadherin and zonula occludens-1 from cell–cell junctions, and the development of actin stress fibres. These results were replicated using human umbilical vein endothelial cells and confirmed by decreased endothelial resistance. Interestingly, we demonstrated that this increased endothelial permeability is a reactive oxygen species (ROS)-dependent mechanism in vitro and in vivo using a cotreatment with an antioxidant agent, N-acetylcysteine.This study shows that dasatinib alters pulmonary endothelial permeability in a ROS-dependent manner in vitro and in vivo leading to pleural effusion.

Sign in / Sign up

Export Citation Format

Share Document