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Prepublished online as a Blood First Edition Paper on October 24, 2002; DOI 10.1182/blood-2002-02-0582. This Article Full Text (PDF) All Versions of this Article: 2002-02-0582v1 101/5/1857    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 Wajih, N. Articles by Sane, D. C Search for Related Content PubMed PubMed Citation Articles by Wajih, N. Articles by Sane, D. C Social Bookmarking                   What's this? Submitted February 22, 2002 Accepted October 15, 2002 Angiostatin selectively inhibits signaling by hepatocyte growth factor in endothelial and smooth muscle cells Nadeem Wajih and David C Sane* Section of Cardiology, Wake Forest University School of Medicine, Winston-Salem, NC, USA * Corresponding author; email: dsane{at}wfubmc.edu. Angiostatin, an inhibitor of angiogenesis, contains 3-4 kringles domains that are derived from proteolytic cleavage of plasminogen. The anti-angiogenic effects of angiostatin occur, in part, from its inhibition of endothelial cell surface ATP synthase, integrin functions and pericellular proteolysis. Angiostatin has structural similarities to hepatocyte growth factor ("scatter factor"), a promoter of angiogenesis, that induces proliferation and migration of both endothelial and smooth muscle cells via its cell surface receptor, c-met. We hypothesized that angiostatin might block HGF-induced signaling in endothelial cells and smooth muscle cells. Angiostatin inhibited HGF-induced phosphorylation of c-met, Akt, and ERK1/2. Angiostatin also significantly inhibited proliferation of HUVEC- induced by HGF. In contrast, angiostatin did not inhibit VEGF- or bFGF-induced signaling events or HUVEC proliferation. Angiostatin bound to immobilized truncated c-met produced by A431 cells and could be immunoprecipitated as a complex with soluble c-met. HGF inhibited the binding of 125I-angiostatin to HUVEC. Soluble c-met, produced by several tumor cell lines, could inhibit the anti-angiogenic effect of angiostatin. The disruption of HGF/c-met signaling is a novel mechanism for the anti-angiogenic effect of angiostatin. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T.-Y. Lee, S. Muschal, E. A. Pravda, J. Folkman, A. Abdollahi, and K. Javaherian Angiostatin regulates the expression of antiangiogenic and proapoptotic pathways via targeted inhibition of mitochondrial proteins Blood, August 27, 2009; 114(9): 1987 - 1998. [Abstract] [Full Text] [PDF] A. Bratt, O. Birot, I. Sinha, N. Veitonmaki, K. Aase, M. Ernkvist, and L. Holmgren Angiomotin Regulates Endothelial Cell-Cell Junctions and Cell Motility J. Biol. Chem., October 14, 2005; 280(41): 34859 - 34869. [Abstract] [Full Text] [PDF] V. Leksa, S. Godar, H. B. Schiller, E. Fuertbauer, A. Muhammad, K. Slezakova, V. Horejsi, P. Steinlein, U. H. Weidle, B. R. Binder, et al. TGF-{beta}-induced apoptosis in endothelial cells mediated by M6P/IGFII-R and mini-plasminogen J. Cell Sci., October 1, 2005; 118(19): 4577 - 4586. [Abstract] [Full Text] [PDF] M. S. Aguzzi, C. Giampietri, F. De Marchis, F. Padula, R. Gaeta, G. Ragone, M. C. Capogrossi, and A. Facchiano RGDS peptide induces caspase 8 and caspase 9 activation in human endothelial cells Blood, June 1, 2004; 103(11): 4180 - 4187. [Abstract] [Full Text] [PDF] J.-H. Ahn, J.-S. Kim, H.-K. Yu, H.-J. Lee, and Y. Yoon A Truncated Kringle Domain of Human Apolipoprotein(a) Inhibits the Activation of Extracellular Signal-regulated Kinase 1 and 2 through a Tyrosine Phosphatase-dependent Pathway J. Biol. Chem., May 21, 2004; 279(21): 21808 - 21814. [Abstract] [Full Text] [PDF] A. Ikai, R. K. Riemer, X. Ma, O. Reinhartz, F. L. Hanley, and V. M. Reddy Pulmonary expression of the hepatocyte growth factor receptor c-Met shifts from medial to intimal layer after cavopulmonary anastomosis J. Thorac. Cardiovasc. Surg., May 1, 2004; 127(5): 1442 - 1449. [Abstract] [Full Text] [PDF] T. Levchenko, K. Aase, B. Troyanovsky, A. Bratt, and L. Holmgren Loss of responsiveness to chemotactic factors by deletion of the C-terminal protein interaction site of angiomotin J. Cell Sci., September 15, 2003; 116(18): 3803 - 3810. [Abstract] [Full Text] [PDF]

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