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J. Biol. Chem., Vol. 281, Issue 21, 14533-14536, May 26, 2006
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1
From the
Departments of
Cell Biology and
Pathology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0006
Angiogenesis is the formation of new blood vessels from the existing vasculature and is necessary for tumor growth. Syndecan-2 (S2) is highly expressed in the microvasculature of mouse gliomas. When S2 expression was down-regulated in mouse brain microvascular endothelial cells (MvEC), this inhibited cell motility and reduced the formation of capillary tube-like structures in vitro. Pro-angiogenic growth factors and enzymes up-regulated during glioma tumorigenesis stimulated shedding of the S2 ectodomain from endothelial cells in vitro. The effect of shed S2 on angiogenic processes was investigated by incorporating recombinant S2 ectodomain (S2ED) into in vitro angiogenesis assays. S2ED promoted membrane protrusion, migration, capillary tube formation, and cell-cell interactions. We therefore propose that S2 is necessary for angiogenesis of MvEC, proangiogenic factors expressed during glioma progression regulate S2 shedding, and shed S2 ectodomain may increase endothelial cell angiogenic processes.
Received for publication, March 23, 2006
* This work was supported by National Institutes of Health (NIH) Grants DK54605 and GM50194 (to A. W.), NIH-NCI Grant CA97110 (to C. L. G.), and NIH-NHLBI Training Grant T32-HL07918 (to C. Y. F.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 To whom correspondence should be addressed: Dept. of Cell Biology, University of Alabama at Birmingham, THT 946, 1530 3rd Ave. South, Birmingham, AL 35294-0006. Tel.: 205-934-1548; Fax: 205-934-7029; and E-mail: anwoods{at}uab.edu.
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