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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 (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 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 Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted June 21, 2005 Accepted September 1, 2005 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 Hematology/Oncology Unit, Department of Medicine, University of Rochester School of Medicine & Dentistry, Rochester, NY, USA Department of Laboratory Animal Medicine, University of Rochester School of Medicine & Dentistry, Rochester, NY, USA * Corresponding author; email: Abha_sahni{at}urmc.rochester.edu. We have shown previously that fibrin(ogen) binds FGF-2 and potentiates stimulation of endothelial cell (EC) proliferation. We have now used two FGF-2 mutants differing only in the five residues constituting the binding site to characterize the importance of this interaction in angiogenesis. The non-binding (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 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 wt-FGF-2 and 221*2, whereas no augmentation occurred with 2212 and fibrinogen. Using a placental explant model in a fibrin matrix, wt-FGF-2 resulted in 2.6 ± 0.9 fold more growth over control, and 221*2 increased growth 3.3 ± 0.9 fold. Vessel outgrowth with 2212 was minimal and comparable to control. Similarly, fibrinogen potentiated wt-FGF-2 or 221*2-mediated angiogenesis in the chicken CAM model. In a mouse Matrigel implant model, fibrinogen significantly increased angiogenesis with either wt-FGF-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 five 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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