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 The vascular endothelial cell-expressed prion protein doppel promotes angiogenesis and blood-brain barrier development

Development ◽  
2020 ◽  
Vol 147 (18) ◽  
pp. dev193094
Author(s):  
Zhihua Chen ◽  
John E. Morales ◽  
Naze Avci ◽  
Paola A. Guerrero ◽  
Ganesh Rao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Blood Vessel ◽  
Prion Protein ◽  
Tyrosine Kinases ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
And Migration ◽  
Migration Analysis

ABSTRACTThe central nervous system (CNS) contains a complex network of blood vessels that promote normal tissue development and physiology. Abnormal control of blood vessel morphogenesis and maturation is linked to the pathogenesis of various neurodevelopmental diseases. The CNS-specific genes that regulate blood vessel morphogenesis in development and disease remain largely unknown. Here, we have characterized functions for the gene encoding prion protein 2 (Prnd) in CNS blood vessel development and physiology. Prnd encodes the glycosylphosphatidylinositol (GPI)-linked protein doppel, which is expressed on the surface of angiogenic vascular endothelial cells, but is absent in quiescent endothelial cells of the adult CNS. During CNS vascular development, doppel interacts with receptor tyrosine kinases and activates cytoplasmic signaling pathways involved in endothelial cell survival, metabolism and migration. Analysis of mice genetically null for Prnd revealed impaired CNS blood vessel morphogenesis and associated endothelial cell sprouting defects. Prnd−/− mice also displayed defects in endothelial barrier integrity. Collectively, these data reveal novel mechanisms underlying doppel control of angiogenesis in the developing CNS, and may provide new insights about dysfunctional pathways that cause vascular-related CNS disorders.

scholarly journals A Relationship between vascular endothelial cell senescence and cardiovascular disease

2021 ◽  
Vol 271 ◽  
pp. 03062
Author(s):  
Ji-Na Qing ◽  
Yan Lei ◽  
Mei-Hua Bao ◽  
Qing-Ming Fu
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Cell ◽  
Blood Vessel ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Vascular Endothelial Cell ◽  
Single Layer ◽  
Vascular Endothelial ◽  
Age Related ◽  
Close Relationship

The vascular endothelial cell (VEC) is a single layer of flat squamous epithelium covering the intima of the blood vessel. It constitutes a biological barrier to the blood vessel wall. It is not only a protective barrier but also a producer of some autocrine secretion. The substance is used to regulate homeostasis and vascular tone and has a variety of biological functions. VEC senescence can lead to vascular dysfunction, which is a major risk factor for cardiovascular system (CVS) and has a close relationship with cardiovascular disease (CVD). However, the mechanism of VEC senescence and the effects of VEC senescence on vascular function are not fully understood. This review summarizes the characteristics of VEC senescence and describes age-related CVD.

Effect of angiotensin(1-7) on the expression of E-selectin induced by angiotensinII and its mechanism in vascular endothelial cell

2010 ◽  
Vol 34 (8) ◽  
pp. S71-S71
Author(s):  
Xiaohui Shen ◽  
Zhi‑Bin Wen ◽  
Na Li ◽  
Qingmei Cheng ◽  
Xiaofan He ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial

Alterations in Vascular Endothelial Cell-related Plasma Proteins In Thalassaemic Patients and their Correlation with Clinical Symptoms

1995 ◽  
Vol 74 (04) ◽  
pp. 1045-1049 ◽  
Author(s):  
P Butthep ◽  
A Bunyaratvej ◽  
Y Funahara ◽  
H Kitaguchi ◽  
S Fucharoen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Immunosorbent Assay ◽  
Plasma Proteins ◽  
Clinical Symptoms ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Vascular Endothelial ◽  
Leg Ulcers

SummaryAn increased level of plasma thrombomodulin (TM) in α- and β- thalassaemia was demonstrated using an enzyme-linked immunosorbent assay (ELISA). Nonsplenectomized patients with β-thalassaemia/ haemoglobin E (BE) had higher levels of TM than splenectomized cases (BE-S). Patients with leg ulcers (BE-LU) were found to have the highest increase in TM level. Appearance of larger platelets in all types of thalassaemic blood was observed indicating an increase in the number of younger platelets. These data indicate that injury of vascular endothelial cells is present in thalassaemic patients.

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