ArticleThe Journal of cell biology1998
Receptor-independent role of urokinase-type plasminogen activator in pericellular plasmin and matrix metalloproteinase proteolysis during vascular wound healing in mice.
Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 130 citations in OpenAlex.
- Plasmin activity promotes amyloid deposition in a transgenic model of human transthyretin amyloidosis.Nature communications · 2021Article
- The Urokinase Receptor (uPAR) as a "Trojan Horse" in Targeted Cancer Therapy: Challenges and Opportunities.Cancers · 2021Review
- Urokinase-type plasminogen activator-mediated crosstalk between N-cadherin and β-catenin promotes wound healing.Journal of cell science · 2021Article
- Therapeutics targeting the fibrinolytic system.Experimental & molecular medicine · 2020Review
- Contribution of platelets, the coagulation and fibrinolytic systems to cutaneous wound healing.Thrombosis research · 2019Review
- TEM8 functions as a receptor for uPA and mediates uPA-stimulated EGFR phosphorylation.Cell communication and signaling : CCS · 2018Article
- D2A sequence of the urokinase receptor induces cell growth through αvβ3 integrin and EGFR.Cellular and molecular life sciences : CMLS · 2018Article
- Article
- MHJ_0461 is a multifunctional leucine aminopeptidase on the surface of Mycoplasma hyopneumoniae.Open biology · 2015Article
- Molecular functions of thyroid hormones and their clinical significance in liver-related diseases.BioMed research international · 2013Review
- A novel autologous cell-based therapy to promote diabetic wound healing.Annals of surgery · 2012Article
- Urokinase-type plasminogen activator-like proteases in teleosts lack genuine receptor-binding epidermal growth factor-like domains.The Journal of biological chemistry · 2012Article
- Urokinase-type plasminogen activator deficiency in bone marrow-derived cells augments rupture of angiotensin II-induced abdominal aortic aneurysms.Arteriosclerosis, thrombosis, and vascular biology · 2011Article
- Article
- Down-regulation of uPA and uPAR by 3,3'-diindolylmethane contributes to the inhibition of cell growth and migration of breast cancer cells.Journal of cellular biochemistry · 2009Article
- Inactivation of uPA and its receptor uPAR by 3,3'-diindolylmethane (DIM) leads to the inhibition of prostate cancer cell growth and migration.Journal of cellular biochemistry · 2009Article
- Impact of plasminogen on an in vitro wound healing model based on a perfusion cell culture system.Molecular and cellular biochemistry · 2009Article
- Dissecting the urokinase activation pathway using urokinase-activated anthrax toxin.Methods in molecular biology (Clifton, N.J.) · 2009Article
- Immunomodulatory effects of plasminogen activators on hepatic fibrogenesis.Clinical and experimental immunology · 2008Article
- uPA deficiency exacerbates muscular dystrophy in MDX mice.The Journal of cell biology · 2007Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been proposed that the urokinase receptor (u-PAR) is essential for the various biological roles of urokinase-type plasminogen activator (u-PA) in vivo, and that smooth muscle cells require u-PA for migration during arterial neointima formation. The present study was undertaken to evaluate the role of u-PAR during this process in mice with targeted disruption of the u-PAR gene (u-PAR-/-). Surprisingly, u-PAR deficiency did not affect arterial neointima formation, neointimal cell accumulation, or migration of smooth muscle cells. Indeed, topographic analysis of arterial wound healing after electric injury revealed that u-PAR-/- smooth muscle cells, originating from the uninjured borders, migrated over a similar distance and at a similar rate into the necrotic center of the wound as wild-type (u-PAR+/+) smooth muscle cells. In addition, u-PAR deficiency did not impair migration of wounded cultured smooth muscle cells in vitro. There were no genotypic differences in reendothelialization of the vascular wound. The minimal role of u-PAR in smooth muscle cell migration was not because of absent expression, since wild-type smooth muscle cells expressed u-PAR mRNA and functional receptor in vitro and in vivo. Pericellular plasmin proteolysis, evaluated by degradation of 125I-labeled fibrin and activation of zymogen matrix metalloproteinases, was similar for u-PAR-/- and u-PAR+/+ cells. Immunoelectron microscopy of injured arteries in vivo revealed that u-PA was bound on the cell surface of u-PAR+/+ cells, whereas it was present in the pericellular space around u-PAR-/- cells. Taken together, these results suggest that binding of u-PA to u-PAR is not required to provide sufficient pericellular u-PA-mediated plasmin proteolysis to allow cellular migration into a vascular wound.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.