The fibrinogen globe of tenascin-C promotes basic fibroblast growth factor-induced endothelial cell elongation

To investigate the potential role of tenascin-C (TN-C) on endothelial sprou ting we used bovine aortic endothelial cells (BAECs) as an in vitro model o f angiogenesis. We found that TN-C is specifically expressed by sprouting a nd cord-forming BAECs but not by nonsprouting BAECs. To test whether TN-C a lone or in combination with basic fibroblast growth factor (bFGF) can enhan ce 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, ex ogenous TN-C but not fibronectin induced an elongated phenotype in nonsprou ting BAECs. This phenotype was due to altered actin cytoskeleton organizati on. The fibrinogen globe of the TN-C molecule was the active domain promoti ng 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.