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Angiostatin induces endothelial cell apoptosis and activation of focal adhesion kinase independently of the integrin-binding motif RGD
Author(s) -
Lena ClaessonWelsh,
Michael Welsh,
Nobuyuki Ito,
Bela AnandApte,
Shay Söker,
Bruce R. Zetter,
Michael S. O’Reilly,
Judah Folkman
Publication year - 1998
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.95.10.5579
Subject(s) - angiostatin , focal adhesion , microbiology and biotechnology , integrin , angiogenesis , cell adhesion , endothelial stem cell , chemistry , signal transduction , cancer research , biology , cell , biochemistry , in vitro
Angiostatin, a fragment of plasminogen, has been identified and characterized as an endogenous inhibitor of neovascularization. We show that angiostatin treatment of endothelial cells in the absence of growth factors results in an increased apoptotic index whereas the proliferation index is unchanged. Angiostatin also inhibits migration and tube formation of endothelial cells. Angiostatin treatment has no effect on growth factor-induced signal transduction but leads to an RGD-independent induction of the kinase activity of focal adhesion kinase, suggesting that the biological effects of angiostatin relate to subversion of adhesion plaque formation in endothelial cells.

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