TEM8 expression stimulates endothelial cell adhesion and migration by regulating cell?matrix interactions on collagen

2005 ◽  
Vol 305 (1) ◽  
pp. 133-144 ◽  
Author(s):  
K HOTCHKISS ◽  
C BASILE ◽  
S SPRING ◽  
G BONUCCELLI ◽  
M LISANTI ◽  
...  
Oncotarget ◽  
2016 ◽  
Vol 7 (9) ◽  
pp. 10090-10103 ◽  
Author(s):  
Federico Galvagni ◽  
Federica Nardi ◽  
Marco Maida ◽  
Giulia Bernardini ◽  
Silvia Vannuccini ◽  
...  

2002 ◽  
Vol 277 (19) ◽  
pp. 17281-17290 ◽  
Author(s):  
Gieri Camenisch ◽  
Maria Teresa Pisabarro ◽  
Daniel Sherman ◽  
Joe Kowalski ◽  
Mark Nagel ◽  
...  

Author(s):  
Abdullah A. A. Alghamdi ◽  
Christopher J. Benwell ◽  
Samuel J. Atkinson ◽  
Jordi Lambert ◽  
Robert T. Johnson ◽  
...  

Biomaterials ◽  
2012 ◽  
Vol 33 (7) ◽  
pp. 1959-1969 ◽  
Author(s):  
Juliane Teichmann ◽  
Alexander Morgenstern ◽  
Jochen Seebach ◽  
Hans-Joachim Schnittler ◽  
Carsten Werner ◽  
...  

Pharmacology ◽  
2010 ◽  
Vol 85 (3) ◽  
pp. 136-145 ◽  
Author(s):  
Hua Li ◽  
Li-jun Zhang ◽  
Bai-hua Chen ◽  
Xuan Zhou ◽  
Ke Su ◽  
...  

2010 ◽  
Vol 299 (6) ◽  
pp. C1468-C1484 ◽  
Author(s):  
SunYoung Park ◽  
Terri A. DiMaio ◽  
Elizabeth A. Scheef ◽  
Christine M. Sorenson ◽  
Nader Sheibani

Platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) is a member of the immunoglobulin superfamily of cell adhesion molecules with important roles in angiogenesis and inflammation. However, the molecular and cellular mechanisms, and the role that specific PECAM-1 isoforms play in these processes, remain elusive. We recently showed attenuation of retinal vascular development and neovascularization in PECAM-1-deficient (PECAM-1−/−) mice. To gain further insight into the role of PECAM-1 in these processes, we isolated primary retinal endothelial cells (EC) from wild-type (PECAM-1+/+) and PECAM-1−/− mice. Lack of PECAM-1 had a significant impact on endothelial cell-cell and cell-matrix interactions, resulting in attenuation of cell migration and capillary morphogenesis. Mechanistically these changes were associated with a significant decrease in expression of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) bioavailability in PECAM-1−/− retinal EC. PECAM-1−/− retinal EC also exhibited a lower rate of apoptosis under basal and challenged conditions, consistent with their increased growth rate. Furthermore, reexpression of PECAM-1 was sufficient to restore migration and capillary morphogenesis of null cells in an isoform-specific manner. Thus PECAM-1 expression modulates proangiogenic properties of EC, and these activities are significantly influenced by alternative splicing of its cytoplasmic domain.


2011 ◽  
Vol 414 (4) ◽  
pp. 750-755 ◽  
Author(s):  
Matthieu Rousseau ◽  
Marie-Hélène Gaugler ◽  
Audrey Rodallec ◽  
Stéphanie Bonnaud ◽  
François Paris ◽  
...  

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