Abstract：
:In vitro experimental evidences suggest that the proteolytic degradation of the extracellular matrix (ECM) by activation of the urokinase-type plasminogen activator (uPA)/plasmin system may affect growth factor activity and bioavailability. However, no direct in vivo observations were available to support this hypothesis. Here we demonstrate that endothelial GM 7373 cells overexpressing human uPA (uPA-R5 cells) cause the release of (125)I-labeled fibroblast growth factor-2 (FGF2) from endothelial ECM in a plasmin-dependent manner. Accordingly, uPA-R5 cells are angiogenic in vivo when applied on the top of the chorioallantoic membrane (CAM) of the chick embryo. In contrast, mock-transfected Neo2 cells are unable to release ECM-bound (125)I-FGF2 and are poorly angiogenic. Neovascularization elicited by uPA-R5 cells is significantly reduced by neutralizing anti-FGF2 antibodies to values similar to those observed in Neo2 cell-treated CAMs. Accordingly, purified human uPA stimulates neovascularization of the CAM in the absence of an inflammatory response. The angiogenic activity of uPA is significantly inhibited by neutralizing anti-FGF2 antibodies or by pretreatment with phenylmethylsulfonyl fluoride. The non-catalytic, receptor-binding amino-terminal fragment of uPA is instead non angiogenic. Taken together, the data indicate that uPA is able to induce angiogenesis in vivo via a plasmin-dependent degradation of ECM that causes the mobilization of stored endogenous FGF2.
journal_name
J Cell Scijournal_title
Journal of cell scienceauthors
Ribatti D,Leali D,Vacca A,Giuliani R,Gualandris A,Roncali L,Nolli ML,Presta Mkeywords:
subject
Has Abstractpub_date
1999-12-01 00:00:00pages
4213-21eissn
0021-9533issn
1477-9137journal_volume
112 ( Pt 23)pub_type
杂志文章abstract：:A new aspect of research into the pathogenesis of cystic fibrosis (CF) is a genetics-based search for ;modifier genes' that may affect the severity of CF lung disease. Using an alternative, cell biological approach, we show that ITPK1 should be considered a modifier gene. ITPK1 synthesizes an intracellular signal, ino...
journal_title：Journal of cell science
pub_type： 杂志文章
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更新日期：2011-04-01 00:00:00
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更新日期：2009-10-15 00:00:00
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pub_type： 杂志文章
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更新日期：2021-01-08 00:00:00
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journal_title：Journal of cell science
pub_type： 杂志文章
doi：
更新日期：1993-05-01 00:00:00
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journal_title：Journal of cell science
pub_type： 杂志文章
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更新日期：2011-04-01 00:00:00
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pub_type： 杂志文章,评审
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更新日期：2013-12-01 00:00:00
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journal_title：Journal of cell science
pub_type： 杂志文章
doi：
更新日期：1993-12-01 00:00:00
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更新日期：2011-08-01 00:00:00
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journal_title：Journal of cell science
pub_type： 杂志文章
doi：
更新日期：2001-12-01 00:00:00
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journal_title：Journal of cell science
pub_type： 杂志文章
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更新日期：1994-06-01 00:00:00
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journal_title：Journal of cell science
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doi：
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更新日期：1980-04-01 00:00:00
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journal_title：Journal of cell science
pub_type： 杂志文章
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更新日期：2000-09-01 00:00:00
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journal_title：Journal of cell science
pub_type： 杂志文章
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更新日期：2003-07-01 00:00:00
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pub_type： 杂志文章
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