Winderlich, Mark; Keller, Linda; Cagna, Giuseppe; Broermann, Andre; Kamenyeva, Olena; Kiefer, Friedemann; Deutsch, Urban; Nottebaum, Astrid F; Vestweber, Dietmar (2009). VE-PTP controls blood vessel development by balancing Tie-2 activity. Journal of cell biology, 185(4), pp. 657-71. New York, N.Y.: Rockefeller Institute Press 10.1083/jcb.200811159
Full text not available from this repository.Vascular endothelial protein tyrosine phosphatase (VE-PTP) is an endothelial-specific receptor-type tyrosine phosphatase that associates with Tie-2 and VE-cadherin. VE-PTP gene disruption leads to embryonic lethality, vascular remodeling defects, and enlargement of vascular structures in extraembryonic tissues. We show here that antibodies against the extracellular part of VE-PTP mimic the effects of VE-PTP gene disruption exemplified by vessel enlargement in allantois explants. These effects require the presence of the angiopoietin receptor Tie-2. Analyzing the mechanism we found that anti-VE-PTP antibodies trigger endocytosis and selectively affect Tie-2-associated, but not VE-cadherin-associated VE-PTP. Dissociation of VE-PTP triggers the activation of Tie-2, leading to enhanced endothelial cell proliferation and enlargement of vascular structures through activation of Erk1/2. Importantly, the antibody effect on vessel enlargement is also observed in newborn mice. We conclude that VE-PTP is required to balance Tie-2 activity and endothelial cell proliferation, thereby controlling blood vessel development and vessel size.
Item Type: |
Journal Article (Original Article) |
|---|---|
Division/Institute: |
04 Faculty of Medicine > Pre-clinic Human Medicine > Theodor Kocher Institute |
UniBE Contributor: |
Deutsch, Urban |
ISSN: |
0021-9525 |
Publisher: |
Rockefeller Institute Press |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 15:13 |
Last Modified: |
05 Dec 2022 14:22 |
Publisher DOI: |
10.1083/jcb.200811159 |
PubMed ID: |
19451274 |
Web of Science ID: |
000266279900011 |
URI: |
https://boris.unibe.ch/id/eprint/32151 (FactScience: 197079) |
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