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Research Article Free access | 10.1172/JCI118489

Generation and characterization of urokinase receptor-deficient mice.

M Dewerchin, A V Nuffelen, G Wallays, A Bouché, L Moons, P Carmeliet, R C Mulligan, and D Collen

Center for Transgene Technology and Gene Therapy, Vlaams Interuniversitair Institut voor Biotechnologie, Leuven, Belgium.

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Center for Transgene Technology and Gene Therapy, Vlaams Interuniversitair Institut voor Biotechnologie, Leuven, Belgium.

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Center for Transgene Technology and Gene Therapy, Vlaams Interuniversitair Institut voor Biotechnologie, Leuven, Belgium.

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Center for Transgene Technology and Gene Therapy, Vlaams Interuniversitair Institut voor Biotechnologie, Leuven, Belgium.

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Center for Transgene Technology and Gene Therapy, Vlaams Interuniversitair Institut voor Biotechnologie, Leuven, Belgium.

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Center for Transgene Technology and Gene Therapy, Vlaams Interuniversitair Institut voor Biotechnologie, Leuven, Belgium.

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Center for Transgene Technology and Gene Therapy, Vlaams Interuniversitair Institut voor Biotechnologie, Leuven, Belgium.

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Center for Transgene Technology and Gene Therapy, Vlaams Interuniversitair Institut voor Biotechnologie, Leuven, Belgium.

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Published February 1, 1996 - More info

Published in Volume 97, Issue 3 on February 1, 1996
J Clin Invest. 1996;97(3):870–878. https://doi.org/10.1172/JCI118489.
© 1996 The American Society for Clinical Investigation
Published February 1, 1996 - Version history
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Abstract

Mice homozygously deficient for the urokinase-type plasminogen activator (u-PA) receptor (u-PAR-1-) were generated by homologous recombination in D3, embryonic stem cells. The genomic sequences comprising exon 2 through 5 of the u-PAR gene were replaced by the neomycin resistance gene, resulting in inactivation of both u-PAR splice variants. The inactivated u-PAR allele was transmitted via mendelian inheritance, and fertility. Inactivation of u-PAR was confirmed by the absence of binding of rabbit anti-murine u-PAR or of an aminoterminal fragment of murine u-PA (mu-PA.1-48) to u-PAR-1- embryonic fibroblasts and macrophages. u-PAR-1- mice displayed normal lysis of a murine plasma clot injected via the jugular vein. Invasion of macrophages into the peritoneal cavity after thioglycollate stimulation was similar in u-PAR-1- and u-PAR-1- mice. u-PAR-1- peritoneal macrophages had a threefold decreased initial rate of u-PA-mediated plasminogen activation in vitro but degraded extracellular matrix proteins in vitro as efficiently as u-PAR-1- macrophages.

Version history
  • Version 1 (February 1, 1996): No description
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