scholarly journals Transient phenotypic changes in endothelial cells and pericytes in neonatal mouse retina following short-term blockade of vascular endothelial growth factor receptors

2018 ◽  
Vol 247 (5) ◽  
pp. 699-711 ◽  
Author(s):  
Akane Morita ◽  
Asami Mori ◽  
Shiho Arima ◽  
Kenji Sakamoto ◽  
Tohru Nagamitsu ◽  
...  





Neurosurgery ◽  
2009 ◽  
Vol 64 (1) ◽  
pp. 139-148 ◽  
Author(s):  
Mark N. Jabbour ◽  
James B. Elder ◽  
Christian G. Samuelson ◽  
Shabnam Khashabi ◽  
Florence M. Hofman ◽  
...  

Abstract OBJECTIVE To identify and characterize the phenotypic and functional differences of endothelial cells derived from cerebral arteriovenous malformations (AVM), as compared with endothelial cells derived from a normal brain. METHODS Isolated AVM brain endothelial cells and control brain endothelial cells were evaluated immunohistochemically for expression of the endothelial cell markers von Willebrand factor and CD31, as well as angiogenic factors including vascular endothelial growth factor A, interleukin-8, and endothelin-1. Vascular endothelial growth factor receptors 1 and 2 were also evaluated using immunohistochemistry techniques. Functional assays evaluated cell proliferation, cytokine production, tubule formation, and cell migration using the modified Boyden chamber technique. RESULTS Endothelial cells derived from AVMs expressed high levels of vascular endothelial growth factor A and significantly overexpressed the vascular endothelial growth factor receptors 1 and 2 (P < 0.05), as compared with control endothelial cells. In addition, comparison to control brain endothelial cells demonstrated that AVM brain endothelial cells proliferated faster, migrated more quickly, and produced aberrant tubule-like structures. CONCLUSION Endothelial cells derived from cerebral AVMs are highly activated cells overexpressing proangiogenic growth factors and exhibiting abnormal functions consistent with highly activated endothelial cells.





1996 ◽  
Vol 271 (10) ◽  
pp. 5519-5523 ◽  
Author(s):  
Hela Gitay-Goren ◽  
Tzafra Cohen ◽  
Shoshana Tessler ◽  
Shay Soker ◽  
Stela Gengrinovitch ◽  
...  


2001 ◽  
Vol 21 (14) ◽  
pp. 4647-4655 ◽  
Author(s):  
Iiro Rajantie ◽  
Niklas Ekman ◽  
Kristiina Iljin ◽  
Elena Arighi ◽  
Yuji Gunji ◽  
...  

ABSTRACT The Bmx gene, a member of the Tec tyrosine kinase gene family, is known to be expressed in subsets of hematopoietic and endothelial cells. In this study, mice were generated in which the first coding exon of the Bmx gene was replaced with thelacZ reporter gene by a knock-in strategy. The homozygous mice lacking Bmx activity were fertile and had a normal life span without an obvious phenotype. Staining of their tissues using β-galactosidase substrate to assess the sites ofBmx expression revealed strong signals in the endothelial cells of large arteries and in the endocardium starting between days 10.5 and 12.5 of embryogenesis and continuing in adult mice, while the venular endothelium showed a weak signal only in the superior and inferior venae cavae. Of the five known endothelial receptor tyrosine kinases tested, activated Tie-2 induced tyrosyl phosphorylation of the Bmx protein and both Tie-2 and vascular endothelial growth factor receptor 1 (VEGFR-1) stimulated Bmx tyrosine kinase activity. Thus, the Bmx tyrosine kinase has a redundant role in arterial endothelial signal transduction downstream of the Tie-2 and VEGFR-1 growth factor receptors.



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