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Matrix metalloproteinase-19 inhibits growth of endothelial cells by generating angiostatin-like fragments from plasminogen
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SYSNO ASEP 0371282 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Matrix metalloproteinase-19 inhibits growth of endothelial cells by generating angiostatin-like fragments from plasminogen Author(s) Brauer, Rena (UMG-J)
Beck, Inken (BTO-N)
Roderfeld, M. (DE)
Roeb, E. (DE)
Sedláček, Radislav (UMG-J) RIDSource Title BMC Biochemistry - ISSN 1471-2091
Roč. 12, - (2011), e38Number of pages 8 s. Language eng - English Country GB - United Kingdom Keywords matrix metalloproteinase-19 ; angiogenesis ; endothelial cells Subject RIV EB - Genetics ; Molecular Biology R&D Projects GC301/08/J053 GA ČR - Czech Science Foundation (CSF) GP301/09/P662 GA ČR - Czech Science Foundation (CSF) CEZ AV0Z50520701 - BTO-N (2007-2013) AV0Z50520514 - UMG-J (2005-2011) UT WOS 000294281100001 DOI 10.1186/1471-2091-12-38 Annotation We report here that MMP-19 processes human plasminogen in a characteristic cleavage pattern to generate three angiostatin-like fragments with a molecular weight of 35, 38, and 42 kDa. These fragments released by MMP-19 significantly inhibited the proliferation of HMEC cells by 27% (p = 0.01) and reduced formation of capillary-like structures by 45% (p = 0.05) compared with control cells. As it is known that angiostatin blocks hepatocyte growth factor (HGF)-induced pro-angiogenic signaling in endothelial cells due to structural similarities to HGF, we have analyzed if the plasminogen fragments generated by MMP-19 interfere with this pathway. As it involves the activation of c-met, the receptor of HGF, we could show that MMP-19-dependent processing of plasminogen decreases the phosphorylation of c-met. Conclusion: Altogether, MMP-19 exhibits an anti-angiogenic effect on endothelial cells via generation of angiostatin-like fragments. Workplace Institute of Molecular Genetics Contact Nikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217 Year of Publishing 2012
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