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 In vitro release of vascular endothelial growth factor from gadolinium-doped biodegradable microspheres

2004 ◽  
Vol 51 (6) ◽  
pp. 1265-1271 ◽  
Author(s):  
Anthony Z. Faranesh ◽  
Monet T. Nastley ◽  
Cristina Perez de la Cruz ◽  
Michael F. Haller ◽  
Patrice Laquerriere ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
In Vitro Release ◽  
Biodegradable Microspheres ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
Vitro Release

scholarly journals Platelet-Rich Plasma Prevents In Vitro Transforming Growth Factor-β1-Induced Fibroblast to Myofibroblast Transition: Involvement of Vascular Endothelial Growth Factor (VEGF)-A/VEGF Receptor-1-Mediated Signaling †

Cells ◽  
2018 ◽  
Vol 7 (9) ◽  
pp. 142 ◽  
Author(s):  
Flaminia Chellini ◽  
Alessia Tani ◽  
Larissa Vallone ◽  
Daniele Nosi ◽  
Paola Pavan ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Platelet Rich Plasma ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
The Impact ◽  
Tgf Β1

The antifibrotic potential of platelet-rich plasma (PRP) is controversial. This study examined the effects of PRP on in vitro transforming growth factor (TGF)-β1-induced differentiation of fibroblasts into myofibroblasts, the main drivers of fibrosis, and the involvement of vascular endothelial growth factor (VEGF)-A in mediating PRP-induced responses. The impact of PRP alone on fibroblast differentiation was also assessed. Myofibroblastic phenotype was evaluated by confocal fluorescence microscopy and western blotting analyses of α-smooth muscle actin (sma) and type-1 collagen expression, vinculin-rich focal adhesion clustering, and stress fiber assembly. Notch-1, connexin 43, and VEGF-A expression were also analyzed by RT-PCR. PRP negatively regulated fibroblast-myofibroblast transition via VEGF-A/VEGF receptor (VEGFR)-1-mediated inhibition of TGF-β1/Smad3 signaling. Indeed TGF-β1/PRP co-treated fibroblasts showed a robust attenuation of the myofibroblastic phenotype concomitant with a decrease of Smad3 expression levels. The VEGFR-1 inhibition by KRN633 or blocking antibodies, or VEGF-A neutralization in these cells prevented the PRP-promoted effects. Moreover PRP abrogated the TGF-β1-induced reduction of VEGF-A and VEGFR-1 cell expression. The role of VEGF-A signaling in counteracting myofibroblast generation was confirmed by cell treatment with soluble VEGF-A. PRP as single treatment did not induce fibroblast myodifferentiation. This study provides new insights into cellular and molecular mechanisms underpinning PRP antifibrotic action.

scholarly journals Porcine ovarian cortex-derived putative stem cells can differentiate into endothelial cells in vitro

2021 ◽  
Author(s):  
Kamil Wartalski ◽  
Gabriela Gorczyca ◽  
Jerzy Wiater ◽  
Zbigniew Tabarowski ◽  
Małgorzata Duda
Keyword(s):  
Stem Cells ◽  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Primary Component ◽  
Marker Genes ◽  
Vascular Endothelial ◽  
Ovarian Cortex ◽  
Endothelial Growth Factor

AbstractEndothelial cells (ECs), the primary component of the vasculature, play a crucial role in neovascularization. However, the number of endogenous ECs is inadequate for both experimental purposes and clinical applications. Porcine ovarian putative stem cells (poPSCs), although not pluripotent, are characterized by great plasticity. Therefore, this study aimed to investigate whether poPSCs have the potential to differentiate into cells of endothelial lineage. poPSCs were immunomagnetically isolated from postnatal pig ovaries based on the presence of SSEA-4 protein. Expression of mesenchymal stem cells (MSCs) markers after pre-culture, both at the level of mRNA: ITGB1, THY, and ENG and corresponding protein: CD29, CD90, and CD105 were significantly higher compared to the control ovarian cortex cells. To differentiate poPSCs into ECs, inducing medium containing vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), insulin-like growth factor (IGF), epidermal growth factor (EGF), ascorbic acid, and heparin was applied. After 14 days, poPSC differentiation into ECs was confirmed by immunofluorescence staining for vascular endothelial cadherin (VECad) and vascular endothelial growth factor receptor-2 (VEGFR-2). Semi-quantitative WB analysis of these proteins confirmed their high abundance. Additionally, qRT-PCR showed that mRNA expression of corresponding marker genes: CDH5, KDR was significantly higher compared with undifferentiated poPSCs. Finally, EC functional status was confirmed by the migration test that revealed that they were capable of positive chemotaxis, while tube formation assay demonstrated their ability to develop capillary networks. In conclusion, our results provided evidence that poPSCs may constitute the MSC population in the ovary and confirmed that they might be a potential source of ECs for tissue engineering.

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