Endothelial cell origin and migration in embryonic heart and cranial blood vessel development

1991 ◽  
Vol 231 (3) ◽  
pp. 383-395 ◽  
Author(s):  
J. Douglas ◽  
Thomas J. Poole
Keyword(s):  
Endothelial Cell ◽  
Blood Vessel ◽  
Embryonic Heart ◽  
Blood Vessel Development ◽  
Vessel Development ◽  
And Migration

Vascular endothelial cell specific phospho-tyrosine phosphatase (VE-PTP) activity is required for blood vessel development

2006 ◽  
Vol 45 (3) ◽  
pp. 187
Author(s):  
Sebastian Baumer ◽  
Linda Keller ◽  
Astrid Holtmann ◽  
Ruth Funke ◽  
Hartwig Wolburg ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Blood Vessel ◽  
Tyrosine Phosphatase ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Blood Vessel Development ◽  
Vessel Development

scholarly journals VE-PTP controls blood vessel development by balancing Tie-2 activity

2009 ◽  
Vol 185 (4) ◽  
pp. 657-671 ◽  
Author(s):  
Mark Winderlich ◽  
Linda Keller ◽  
Giuseppe Cagna ◽  
Andre Broermann ◽  
Olena Kamenyeva ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Blood Vessel ◽  
Gene Disruption ◽  
Tyrosine Phosphatase ◽  
Endothelial Cell Proliferation ◽  
Newborn Mice ◽  
Blood Vessel Development ◽  
Vascular Structures ◽  
Vessel Development

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.

scholarly journals Rab35 Governs Apicobasal Polarity Through Regulation of Actin Dynamics During Sprouting Angiogenesis

2022 ◽  
Author(s):  
Caitlin R Francis ◽  
Hayle Kincross ◽  
Erich J Kushner
Keyword(s):  
Blood Vessel ◽  
Actin Polymerization ◽  
Tissue Type ◽  
Potential Contribution ◽  
Rab Gtpases ◽  
Sprouting Angiogenesis ◽  
Apicobasal Polarity ◽  
Blood Vessel Development ◽  
Vessel Development ◽  
Sprout Formation

In early blood vessel development, trafficking programs, such as those using Rab GTPases, are tasked with delivering vesicular cargo with high spatiotemporal accuracy. However, the function of many Rab trafficking proteins remain ill-defined in endothelial tissue; therefore, their relevance to blood vessel development is unknown. Rab35 has been shown to play an enigmatic role in cellular behaviors which differs greatly between tissue-type and organism. Importantly, Rab35 has never been characterized for its potential contribution in sprouting angiogenesis; thus, our goal was to map Rab35s primary function in angiogenesis. Our results demonstrate that Rab35 is critical for sprout formation; in its absence apicobasal polarity is entirely lost in vitro and in vivo. To determine mechanism, we systematically explored established Rab35 effectors and show that none are operative in endothelial cells. However, we find that Rab35 partners with DENNd1c, an evolutionarily divergent guanine exchange factor, to localize to actin. Here, Rab35 regulates actin polymerization, which is required to setup proper apicobasal polarity during sprout formation. Our findings establish that Rab35 is a potent regulator of actin architecture during blood vessel development.

scholarly journals Defective blood vessel development and pericyte/pvSMC distribution in α4 integrin-deficient mouse embryos

2006 ◽  
Vol 293 (1) ◽  
pp. 165-177 ◽  
Author(s):  
Alison Grazioli ◽  
Christina S. Alves ◽  
Konstantinos Konstantopoulos ◽  
Joy T. Yang
Keyword(s):  
Blood Vessel ◽  
Mouse Embryos ◽  
Deficient Mouse ◽  
Blood Vessel Development ◽  
Vessel Development
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