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Blood, 1 January 2006, Vol. 107, No. 1, pp. 126-131. Prepublished online as a Blood First Edition Paper on September 13, 2005; DOI 10.1182/blood-2005-06-2460. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-06-2460v1 107/1/126    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Sahni, A. Articles by Francis, C. W. Search for Related Content PubMed PubMed Citation Articles by Sahni, A. Articles by Francis, C. W. Related Collections Hemostasis, Thrombosis, and Vascular Biology Cell Adhesion and Motility Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY FGF-2 binding to fibrin(ogen) is required for augmented angiogenesis Abha Sahni, Alok A. Khorana, Raymond B. Baggs, Hu Peng, and Charles W. Francis From the Hematology/Oncology Unit, Department of Medicine and Department of Laboratory Animal Medicine, University of Rochester School of Medicine and Dentistry Rochester, NY. We have shown previously that fibrin(ogen) binds fibroblast growth factor 2 (FGF-2) and potentiates stimulation of endothelial-cell (EC) proliferation. We have now used 2 FGF-2 mutants differing only in the 5 residues constituting the binding site to characterize the importance of this interaction in angiogenesis. The nonbinding (2212) and binding (221*2) mutants stimulated EC proliferation by 2.2 ± 0.4-fold and 2.9 ± 0.3-fold over control, respectively, and both were similar to wild-type (wt) FGF-2 (2.5 ± 0.3-fold). Proliferation was augmented by fibrinogen to 5.3 ± 1.2-fold and 4.8 ± 0.8-fold with wtFGF-2 and 221*2, whereas no augmentation occurred with 2212 and fibrinogen. Using a placental explant model in a fibrin matrix, wtFGF-2 resulted in 2.6 ± 0.9-fold more growth over control, and 221*2 increased growth 3.3 plus or minus 0.9-fold. Vessel outgrowth with 2212 was minimal and comparable to control. Similarly, fibrinogen potentiated wtFGF-2 or 221*2-mediated angiogenesis in the chicken chorioallantoic membrane model. In a mouse Matrigel implant model, fibrinogen significantly increased angiogenesis with either wtFGF-2 or 221*2, whereas there was no augmentation with 2212. These results demonstrate that binding of FGF-2 to fibrin(ogen) mediated by the 5-residue FGF-2-fibrin(ogen) interactive site is required for augmented angiogenesis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Mori, C.-Y. Wu, S. Yamaji, J. Saegusa, B. Shi, Z. Ma, Y. Kuwabara, K. S. Lam, R. R. Isseroff, Y. K. Takada, et al. Direct Binding of Integrin {alpha}v{beta}3 to FGF1 Plays a Role in FGF1 Signaling J. Biol. Chem., June 27, 2008; 283(26): 18066 - 18075. [Abstract] [Full Text] [PDF] O. B. Goodman Jr., M. Febbraio, R. Simantov, R. Zheng, R. Shen, R. L. Silverstein, and D. M. Nanus Neprilysin Inhibits Angiogenesis via Proteolysis of Fibroblast Growth Factor-2 J. Biol. Chem., November 3, 2006; 281(44): 33597 - 33605. [Abstract] [Full Text] [PDF] E. S. Wijelath, S. Rahman, M. Namekata, J. Murray, T. Nishimura, Z. Mostafavi-Pour, Y. Patel, Y. Suda, M. J. Humphries, and M. Sobel Heparin-II Domain of Fibronectin Is a Vascular Endothelial Growth Factor-Binding Domain: Enhancement of VEGF Biological Activity by a Singular Growth Factor/Matrix Protein Synergism Circ. Res., October 13, 2006; 99(8): 853 - 860. [Abstract] [Full Text] [PDF]

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