Vascular endothelial tyrosine phosphatase (VE-PTP)-null mice undergo vasculogenesis but die embryonically because of defects in angiogenesis Export

@article{citeulike:2910570, abstract = {10.1073/pnas.0611510104 Development of the vascular system depends on the highly coordinated actions of a variety of angiogenic regulators. Several of these regulators are members of the tyrosine kinase superfamily, including VEGF receptors and angiopoietin receptors, Tie1 and Tie2. Tyrosine kinase signaling is counter-regulated by the activity of tyrosine phosphatases, including vascular endothelial protein tyrosine phosphatase (VE-PTP), which has previously been shown to modulate Tie2 activity. We generated mice in which VE-PTP is replaced with a reporter gene. We confirm that VE-PTP is expressed in endothelium and also show that VE-PTP is highly expressed in the developing outflow tract of the heart and later is expressed in developing heart valves. Vasculogenesis occurs normally in mice lacking VE-PTP; however, angiogenesis is abnormal. Angiogenic defects in VE-PTP-null mice were most pronounced in the yolk sac and include a complete failure to elaborate the primitive vascular scaffold into higher-order branched arteries, veins, and capillaries. VE-PTP continues to be expressed into adulthood in the vasculature and heart valves, suggesting later roles in vascular development or homeostasis. VE-PTP is also expressed in the vasculature of growing tumors, suggesting that VE-PTP may be a new potential target for angiogenic therapies.}, author = {Dominguez, Melissa G. and Hughes, Virginia C. and Pan, Li and Simmons, Mary and Daly, Christopher and Anderson, Keith and Noguera-Troise, Irene and Murphy, Andrew J. and Valenzuela, David M. and Davis, Samuel and Thurston, Gavin and Yancopoulos, George D. and Gale, Nicholas W.}, citeulike-article-id = {2910570}, citeulike-linkout-0 = {http://dx.doi.org/10.1073/pnas.0611510104}, citeulike-linkout-1 = {http://www.pnas.org/content/104/9/3243.abstract}, citeulike-linkout-2 = {http://www.pnas.org/content/104/9/3243.full.pdf}, citeulike-linkout-3 = {http://www.pnas.org/cgi/content/abstract/104/9/3243}, citeulike-linkout-4 = {http://view.ncbi.nlm.nih.gov/pubmed/17360632}, citeulike-linkout-5 = {http://www.hubmed.org/display.cgi?uids=17360632}, day = {27}, doi = {10.1073/pnas.0611510104}, journal = {Proceedings of the National Academy of Sciences}, keywords = {angiogenesis, embryo, ve-ptp}, month = {February}, number = {9}, pages = {3243--3248}, posted-at = {2009-11-13 13:41:42}, priority = {2}, title = {Vascular endothelial tyrosine phosphatase (VE-PTP)-null mice undergo vasculogenesis but die embryonically because of defects in angiogenesis}, url = {http://dx.doi.org/10.1073/pnas.0611510104}, volume = {104}, year = {2007} }

TY - JOUR ID - citeulike:2910570 L3 - citeulike-article-id:2910570 N2 - 10.1073/pnas.0611510104 Development of the vascular system depends on the highly coordinated actions of a variety of angiogenic regulators. Several of these regulators are members of the tyrosine kinase superfamily, including VEGF receptors and angiopoietin receptors, Tie1 and Tie2. Tyrosine kinase signaling is counter-regulated by the activity of tyrosine phosphatases, including vascular endothelial protein tyrosine phosphatase (VE-PTP), which has previously been shown to modulate Tie2 activity. We generated mice in which VE-PTP is replaced with a reporter gene. We confirm that VE-PTP is expressed in endothelium and also show that VE-PTP is highly expressed in the developing outflow tract of the heart and later is expressed in developing heart valves. Vasculogenesis occurs normally in mice lacking VE-PTP; however, angiogenesis is abnormal. Angiogenic defects in VE-PTP-null mice were most pronounced in the yolk sac and include a complete failure to elaborate the primitive vascular scaffold into higher-order branched arteries, veins, and capillaries. VE-PTP continues to be expressed into adulthood in the vasculature and heart valves, suggesting later roles in vascular development or homeostasis. VE-PTP is also expressed in the vasculature of growing tumors, suggesting that VE-PTP may be a new potential target for angiogenic therapies. IS - 9 JF - Proceedings of the National Academy of Sciences EP - 3248 TI - Vascular endothelial tyrosine phosphatase (VE-PTP)-null mice undergo vasculogenesis but die embryonically because of defects in angiogenesis VL - 104 SP - 3243 KW - angiogenesis KW - embryo KW - ve-ptp AU - Dominguez, Melissa AU - Hughes, Virginia AU - Pan, Li AU - Simmons, Mary AU - Daly, Christopher AU - Anderson, Keith AU - Noguera-Troise, Irene AU - Murphy, Andrew AU - Valenzuela, David AU - Davis, Samuel AU - Thurston, Gavin AU - Yancopoulos, George AU - Gale, Nicholas PY - 2007/02/27/ UR - http://dx.doi.org/10.1073/pnas.0611510104 ER -