Vascular Endothelial Tyrosine Phosphatase (Ve-ptp)-null Mice Undergo Vasculogenesis but Die Embryonically Because of Defects in Angiogenesis.
From: Regeneron Pharmaceuticals, Inc., 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.
Proceedings of the National Academy of Sciences of the United States of America
- Publish Date: Feb 2007
- ISSN: 0027-8424
- Volume: 104
- Issue: 9
- Pages: 3243-8
- Medium: Print
- Language: English
- Citation (JAMA): Dominguez Melissa G, Hughes Virginia C, Pan Li, et al. Vascular Endothelial Tyrosine Phosphatase (Ve-ptp)-null Mice Undergo Vasculogenesis but Die Embryonically Because of Defects in Angiogenesis.. Proc. Natl. Acad. Sci. U.S.A. Feb 2007;104:3243-8
Abstract
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.
Mesh Headings (Keywords): Animals, Blood Vessels, DNA Primers, Endothelial Cells, Gene Deletion, Gene Targeting, Heart Valves, Lac Operon, Mice, Neovascularization, Physiologic, Protein Tyrosine Phosphatases, Receptor-Like Protein Tyrosine Phosphatases, Class 3, Reverse Transcriptase Polymerase Chain Reaction, Yolk Sac
Check for Full Text / PubMed Unique Identifier (PMID): 17360632
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