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Abstract
Some polyphenols have been shown to inhibit, at physiological levels, the VEGF-induced VEGF receptor-2 signaling that causes angiogenesis, allegedly by direct interaction with VEGF and reducing the binding to its receptor VEGFR2. Surface plasmon resonance was used to measure the parameters of binding between VEGF and polyphenols as well as the nature of the interactions by assessing the effect of physico-chemical changes in the solution. CD spectrometry was used to determine any change in the secondary structure of the protein upon binding. The kinetic parameters (ka, kd, and KD) that characterise the binding to VEGF were measured for both inhibitor and non-inhibitor polyphenolic molecules. The effect of changes in the physico-chemical conditions of the solution where the binding occurred indicated that the nature of the interactions between VEGF and EGCG was predominantly of a hydrophobic nature. CD studies suggested that a change in the secondary structure of the protein occurred upon binding. Direct interaction and binding between VEGF and polyphenol molecules acting as inhibitors of the signaling of VEGFR2 has been measured for the first time. The binding between VEGF and EGCG seemed to be based on hydrophobic interactions and caused a change in the secondary structure of the protein.
Highlights
IntroductionAngiogenesis is a biological process where new blood vessels form from pre-existing ones
Angiogenesis is a biological process where new blood vessels form from pre-existing ones. physiological angiogenesis is a vital and essential process in growth and development, angiogenesis underpins pathological processes such as the growth of tumours and atherosclerotic plaques
Angiogenesis is regulated by inhibitor and activator molecules that must be balanced to maintain a healthy status, but when the activity of activators like the vascular endothelial growth factor-A (VEGF-A) is excessive, it can act as a powerful angiogenic agent and promote growth of diseased tissues
Summary
Angiogenesis is a biological process where new blood vessels form from pre-existing ones. Physiological angiogenesis is a vital and essential process in growth and development, angiogenesis underpins pathological processes such as the growth of tumours and atherosclerotic plaques. Angiogenesis is regulated by inhibitor and activator molecules that must be balanced to maintain a healthy status, but when the activity of activators like the vascular endothelial growth factor-A (VEGF-A) is excessive, it can act as a powerful angiogenic agent and promote growth of diseased tissues (pathological angiogenesis). It has been shown to bind to three receptor tyrosine kinases: VEGF receptor 1 (VEGFR1) which has both positive and negative angiogenic effects; VEGFR2 a primary mediator of the mitogenic, angiogenic, and vascular permeability effects of VEGF-A; and VEGFR3, which is involved in the angiogenesis of lymphatic vessels.
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