QUOTE
English Title: Green tea catechins inhibit VEGF-induced angiogenesis in vitro through suppression of VE-cadherin phosphorylation and inactivation of Akt molecule.
Personal Authors: Tang, F. Y., Nhan Nguyen, Meydani, M.
Author Affiliation: Vascular Biology Laboratory, JM USDA-Human Nutrition Research Center on Aging, Tufts University, 711 Washington Street, Boston, MA 02111, USA.
Editors: No editors
Document Title: International Journal of Cancer, 2003 (Vol. 106) (No. 6) 871-878
Abstract:
Studies have indicated that the consumption of green tea is associated with a reduced risk of developing certain forms of cancer and angiogenesis. The mechanism of inhibition of angiogenesis by green tea or its catechins, however, has not been well-established. Vascular endothelial (VE)-cadherin, an adhesive molecule located at the site of intercellular contact, is involved in cell-cell recognition during vascular morphogenesis. The extracellular domain of VE-cadherin mediates initial cell adhesion, whereas the cytosolic tail binding with β-catenin is required for interaction with the cytoskeleton and junctional strength. Therefore, the cadherin-catenin adhesion system is implicated in cell recognition, differentiation, growth and migration of capillary endothelium. Using tube formation of human microvascular endothelial cells (HMVEC) in culture as an in vitro model of angiogenesis, we reported that vascular endothelial growth factor (VEGF)-induced tube formation is inhibited by anti-VE-cadherin antibody and dose-dependently by green tea catechins. We also demonstrated here that inhibition of tube formation by epigallocatechin gallate (EGCG), one of the green tea catechins, is in part mediated through suppression of VE-cadherin tyrosine phosphorylation and inhibition of Akt activation during VEGF-induced tube formation. These findings indicate that VE-cadherin and Akt, known downstream proteins in VEGFR-2-mediated cascade, are the new-targeted proteins by which green tea catechins inhibit angiogenesis.
http://www.cababstractsplus.org/google/abs...cNo=20043121879
Personal Authors: Tang, F. Y., Nhan Nguyen, Meydani, M.
Author Affiliation: Vascular Biology Laboratory, JM USDA-Human Nutrition Research Center on Aging, Tufts University, 711 Washington Street, Boston, MA 02111, USA.
Editors: No editors
Document Title: International Journal of Cancer, 2003 (Vol. 106) (No. 6) 871-878
Abstract:
Studies have indicated that the consumption of green tea is associated with a reduced risk of developing certain forms of cancer and angiogenesis. The mechanism of inhibition of angiogenesis by green tea or its catechins, however, has not been well-established. Vascular endothelial (VE)-cadherin, an adhesive molecule located at the site of intercellular contact, is involved in cell-cell recognition during vascular morphogenesis. The extracellular domain of VE-cadherin mediates initial cell adhesion, whereas the cytosolic tail binding with β-catenin is required for interaction with the cytoskeleton and junctional strength. Therefore, the cadherin-catenin adhesion system is implicated in cell recognition, differentiation, growth and migration of capillary endothelium. Using tube formation of human microvascular endothelial cells (HMVEC) in culture as an in vitro model of angiogenesis, we reported that vascular endothelial growth factor (VEGF)-induced tube formation is inhibited by anti-VE-cadherin antibody and dose-dependently by green tea catechins. We also demonstrated here that inhibition of tube formation by epigallocatechin gallate (EGCG), one of the green tea catechins, is in part mediated through suppression of VE-cadherin tyrosine phosphorylation and inhibition of Akt activation during VEGF-induced tube formation. These findings indicate that VE-cadherin and Akt, known downstream proteins in VEGFR-2-mediated cascade, are the new-targeted proteins by which green tea catechins inhibit angiogenesis.
http://www.cababstractsplus.org/google/abs...cNo=20043121879
QUOTE
VEGF as a Potential Target for Therapeutic Intervention in Depression
Jennifer L. Warner-Schmidt* and Ronald S. Duman**
*The Rockefeller University, 1230 York Avenue, New York, NY 10065; Email: jschmidt@rockefeller.edu
**Yale University, 34 Park Street, New Haven, CT 06508; Email: ronald.duman@yale.edu
Corresponding Author: Dr. Ronald S. Duman, Email: ronald.duman@yale.edu
Small right arrow pointing to: The publisher's final edited version of this article is available at Curr Opin Pharmacol.
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Summary
Introduction
VEGF in the Central Nervous System: Beyond Angiogenesis
VEGF and Neurogenesis
Behavioral consequences of increased VEGF
VEGF as a therapeutic target for antidepressants
Conclusions
References
Summary
Antidepressants are among the most widely prescribed drugs, however the mechanism underlying their therapeutic efficacy is not known. Neurotrophic factors represent a promising class of targets for antidepressant treatments. We recently characterized a role for vascular endothelial growth factor (VEGF) in cellular and behavioral antidepressant responses. VEGF is a potent mitogen and survival factor for endothelial cells and neurons, and modulator of synaptic transmission. Because VEGF has been implicated in a variety of diseases, understanding the molecular and cellular specificity of antidepressant-induced VEGF will be critical to determine its potential as a therapeutic target in depression.
http://www.pubmedcentral.nih.gov/articlere...i?artid=2259283
Jennifer L. Warner-Schmidt* and Ronald S. Duman**
*The Rockefeller University, 1230 York Avenue, New York, NY 10065; Email: jschmidt@rockefeller.edu
**Yale University, 34 Park Street, New Haven, CT 06508; Email: ronald.duman@yale.edu
Corresponding Author: Dr. Ronald S. Duman, Email: ronald.duman@yale.edu
Small right arrow pointing to: The publisher's final edited version of this article is available at Curr Opin Pharmacol.
Publisher's Disclaimer
Top
>
Summary
Introduction
VEGF in the Central Nervous System: Beyond Angiogenesis
VEGF and Neurogenesis
Behavioral consequences of increased VEGF
VEGF as a therapeutic target for antidepressants
Conclusions
References
Summary
Antidepressants are among the most widely prescribed drugs, however the mechanism underlying their therapeutic efficacy is not known. Neurotrophic factors represent a promising class of targets for antidepressant treatments. We recently characterized a role for vascular endothelial growth factor (VEGF) in cellular and behavioral antidepressant responses. VEGF is a potent mitogen and survival factor for endothelial cells and neurons, and modulator of synaptic transmission. Because VEGF has been implicated in a variety of diseases, understanding the molecular and cellular specificity of antidepressant-induced VEGF will be critical to determine its potential as a therapeutic target in depression.
http://www.pubmedcentral.nih.gov/articlere...i?artid=2259283