Aortic endothelial cells synthesize basic fibroblast growth factor which remains cell associated and platelet-derived growth factor-like protein which is secreted

1987 ◽  
Vol 131 (3) ◽  
pp. 402-408 ◽  
Author(s):  
Israel Vlodavsky ◽  
Rafael Fridman ◽  
Robert Sullivan ◽  
Joachim Sasse ◽  
Michael Klagsbrun
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Platelet Derived Growth Factor ◽  
Fibroblast Growth ◽  
Aortic Endothelial Cells ◽  
Aortic Endothelial

bcl-2 Gene Prevents Apoptosis of Basic Fibroblast Growth Factor-Deprived Murine Aortic Endothelial Cells

1994 ◽  
Vol 213 (2) ◽  
pp. 428-432 ◽  
Author(s):  
Seiji Kondo ◽  
Dali Yin ◽  
Tomokazu Aoki ◽  
Jun A. Takahashi ◽  
Tatsuo Morimura ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
Aortic Endothelial Cells ◽  
Aortic Endothelial

scholarly journals The Fibrinogen Globe of Tenascin-C Promotes Basic Fibroblast Growth Factor-induced Endothelial Cell Elongation

1999 ◽  
Vol 10 (9) ◽  
pp. 2933-2943 ◽  
Author(s):  
Susanne Schenk ◽  
Ruth Chiquet-Ehrismann ◽  
Edouard J. Battegay
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
Aortic Endothelial Cells ◽  
Tenascin C ◽  
Cytoskeleton Organization ◽  
Actin Cytoskeleton Organization

To investigate the potential role of tenascin-C (TN-C) on endothelial sprouting we used bovine aortic endothelial cells (BAECs) as an in vitro model of angiogenesis. We found that TN-C is specifically expressed by sprouting and cord-forming BAECs but not by nonsprouting BAECs. To test whether TN-C alone or in combination with basic fibroblast growth factor (bFGF) can enhance endothelial sprouting or cord formation, we used BAECs that normally do not sprout and, fittingly, do not express TN-C. In the presence of bFGF, exogenous TN-C but not fibronectin induced an elongated phenotype in nonsprouting BAECs. This phenotype was due to altered actin cytoskeleton organization. The fibrinogen globe of the TN-C molecule was the active domain promoting the elongated phenotype in response to bFGF. Furthermore, we found that the fibrinogen globe was responsible for reduced cell adhesion of BAECs on TN-C substrates. We conclude that bFGF-stimulated endothelial cells can be switched to a sprouting phenotype by the decreased adhesive strength of TN-C, mediated by the fibrinogen globe.

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