scholarly journals Lycopene inhibits angiogenesis in human umbilical vein endothelial cells and rat aortic rings

2011 ◽  
Vol 108 (3) ◽  
pp. 431-439 ◽  
Author(s):  
Simone Elgass ◽  
Alan Cooper ◽  
Mridula Chopra
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Inhibitory Effect ◽  
Human Umbilical Vein ◽  
Promising Target ◽  
Tnf Α ◽  
Tumour Vascularisation ◽  
Umbilical Vein Endothelial Cells ◽  
Endothelial Growth Factor

Angiogenesis is important for tumour vascularisation and growth, and is therefore a promising target for cancer therapy. The present study reports inhibition ofin vitroangiogenesis in human umbilical vein endothelial cells (HUVEC) as well as in rat aortic rings at physiological concentrations of lycopene, that is, 1–2 μmol/l. At a final concentration of 1·15 μmol/l, a significant reduction (P < 0·05) in network branching, that is, junction numbers, the number of tubules and tubule length, was observed in both HUVEC as well as in the rat aortic rings. The inhibitory effect of lycopene was independent of the presence of the pro-angiogenic agents, vascular endothelial growth factor and TNF-α. The anti-angiogenic effects of lycopene in the present study were shown at a concentration that should be achievable by dietary means. These results extend our knowledge of one of the putative anti-cancer actions of lycopene.

scholarly journals Interleukin-1βExpression Is Required for Lysophosphatidic Acid-Induced Lymphangiogenesis in Human Umbilical Vein Endothelial Cells

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Chih-Hsin Lin ◽  
JenHer Lu ◽  
Hsinyu Lee
Keyword(s):  
Endothelial Cells ◽  
Lysophosphatidic Acid ◽  
Umbilical Vein ◽  
Tube Formation ◽  
Lipid Mediator ◽  
Vascular Endothelial ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells ◽  
Endothelial Growth Factor

Lysophosphatidic acid (LPA) is a lipid mediator which binds to G-protein-coupled receptors and regulates various cellular responses, including inflammation of endothelial cells. Interleukin- (IL-) 1β, a proinflammatory cytokine, is elevated upon LPA treatment in human umbilical vein endothelial cells (HUVECs). Previous studies indicated that LPA upregulates vascular endothelial growth factor- (VEGF-) C and lymphatic marker expressions in HUVECs. However, the relationships between LPA-induced VEGF-C and IL-1βexpressions are not clear. In this paper, we demonstrated that, in the presence of AF12198, an inhibitor of the IL-1 receptor abolished LPA-induced VEGF-C and lymphatic marker expressions in HUVECs. Furthermore, LPA-inducedin vitrotube formation of HUVECs was also suppressed by pretreatment with AF12198. Our results suggest that LPA-stimulated lymphangiogenesis in HUVECs is mediated through IL-1β-induced VEGF-C expression.

scholarly journals Inhibitory effect of brassinin on TNF-α-induced vascular inflammation in human umbilical vein endothelial cells

2017 ◽  
Vol 16 (5) ◽  
pp. 6890-6895 ◽  
Author(s):  
Byung Hyuk Han ◽  
Jung Joo Yoon ◽  
Eun Sik Choi ◽  
Da Hye Jeong ◽  
Yun Jung Lee ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Vascular Inflammation ◽  
Inhibitory Effect ◽  
Human Umbilical Vein ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells

scholarly journals Effect of TNFα stimulation on expression of kidney risk inflammatory proteins in human umbilical vein endothelial cells cultured in hyperglycemia

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Zaipul I. Md Dom ◽  
Caterina Pipino ◽  
Bozena Krolewski ◽  
Kristina O’Neil ◽  
Eiichiro Satake ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Systemic Exposure ◽  
In Vitro Study ◽  
Human Umbilical Vein ◽  
Intracellular Fraction ◽  
Inflammatory Proteins ◽  
Umbilical Vein Endothelial Cells ◽  
Extracellular Fraction

AbstractWe recently identified a kidney risk inflammatory signature (KRIS), comprising 6 TNF receptors (including TNFR1 and TNFR2) and 11 inflammatory proteins. Elevated levels of these proteins in circulation were strongly associated with risk of the development of end-stage kidney disease (ESKD) during 10-year follow-up. It has been hypothesized that elevated levels of these proteins in circulation might reflect (be markers of) systemic exposure to TNFα. In this in vitro study, we examined intracellular and extracellular levels of these proteins in human umbilical vein endothelial cells (HUVECs) exposed to TNFα in the presence of hyperglycemia. KRIS proteins as well as 1300 other proteins were measured using the SOMAscan proteomics platform. Four KRIS proteins (including TNFR1) were down-regulated and only 1 protein (IL18R1) was up-regulated in the extracellular fraction of TNFα-stimulated HUVECs. In the intracellular fraction, one KRIS protein was down-regulated (CCL14) and 1 protein was up-regulated (IL18R1). The levels of other KRIS proteins were not affected by exposure to TNFα. HUVECs exposed to a hyperglycemic and inflammatory environment also showed significant up-regulation of a distinct set of 53 proteins (mainly in extracellular fraction). In our previous study, circulating levels of these proteins were not associated with progression to ESKD in diabetes.

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