Docosahexaenoic Acid Inhibits Vascular Endothelial Growth Factor (VEGF)-Induced Cell Migration via the GPR120/PP2A/ERK1/2/eNOS Signaling Pathway in Human Umbilical Vein Endothelial Cells

2014 ◽  
Vol 62 (18) ◽  
pp. 4152-4158 ◽  
Author(s):  
Che-Yi Chao ◽  
Chong-Kuei Lii ◽  
Siou-Yu Ye ◽  
Chien-Chun Li ◽  
Chia-Yang Lu ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Cell Migration ◽  
Growth Factor ◽  
Docosahexaenoic Acid ◽  
Signaling Pathway ◽  
Umbilical Vein ◽  
Vascular Endothelial ◽  
Umbilical Vein Endothelial Cells ◽  
Endothelial Growth Factor

Vascular endothelial growth factor–stimulated endothelial cells promote adhesion and activation of platelets

Blood ◽  
2000 ◽  
Vol 96 (13) ◽  
pp. 4216-4221 ◽  
Author(s):  
Henk M. W. Verheul ◽  
Anita S. Jorna ◽  
Klaas Hoekman ◽  
Henk J. Broxterman ◽  
Martijn F. B. G. Gebbink ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Platelet Adhesion ◽  
Umbilical Vein ◽  
Vascular Endothelial ◽  
High Affinity Binding Site ◽  
Umbilical Vein Endothelial Cells ◽  
Endothelial Growth Factor

Abstract Coagulation abnormalities, including an increased platelet turnover, are frequently found in patients with cancer. Because platelets secrete angiogenic factors on activation, this study tested the hypothesis that platelets contribute to angiogenesis. Stimulation with vascular endothelial growth factor (VEGF, 25 ng/mL) of human umbilical vein endothelial cells (HUVECs) promoted adhesion of nonactivated platelets 2.5-fold. In contrast, stimulation of HUVECs with basic fibroblast growth factor (bFGF) did not promote platelet adhesion. By blocking tissue factor (TF) activity, platelet adhesion was prevented and antibodies against fibrin(ogen) and the platelet-specific integrin, αIIbβ3, inhibited platelet adhesion for 70% to 90%. These results indicate that VEGF-induced platelet adhesion to endothelial cells is dependent on activation of TF. The involvement of fibrin(ogen) and the αIIbβ3 integrin, which exposes a high-affinity binding site for fibrin(ogen) on platelet activation, indicates that these adhering platelets are activated. This was supported by the finding that the activity of thrombin, a product of TF-activated coagulation and a potent platelet activator, was required for platelet adhesion. Finally, platelets at physiologic concentrations stimulated proliferation of HUVECs, indicative of proangiogenic activity in vivo. These results support the hypothesis that platelets contribute to tumor-induced angiogenesis. In addition, they may explain the clinical observation of an increased platelet turnover in cancer patients. Platelets may also play an important role in other angiogenesis-dependent diseases in which VEGF is involved, such as diabetes and autoimmune diseases.

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