ArticleThe American journal of pathology1999
Role and localization of urokinase receptor in the formation of new microvascular structures in fibrin matrices.
Article in The American journal of pathology, 1999. 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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Who cites it
23 citing papers in PubMed, 93 citations in OpenAlex.
- A local uPAR-plasmin-TGFβ1 positive feedback loop in a qualitative computational model of angiogenic sprouting explains the in vitro effect of fibrinogen variants.PLoS computational biology · 2018Article
- HIF-2α Expression Regulates Sprout Formation into 3D Fibrin Matrices in Prolonged Hypoxia in Human Microvascular Endothelial Cells.PloS one · 2016Article
- Specific effects of fibrinogen and the γA and γ'-chain fibrinogen variants on angiogenesis and wound healing.Tissue engineering. Part A · 2015Article
- Sculpting the blank slate: how fibrin's support of vascularization can inspire biomaterial design.Acta biomaterialia · 2014Review
- Using Del-1 to tip the angiogenic balance in endothelial cells in modular constructs.Tissue engineering. Part A · 2014Article
- Bone marrow-derived mesenchymal stem cells enhance angiogenesis via their α6β1 integrin receptor.Experimental cell research · 2013Article
- High concentration of urokinase-type plasminogen activator receptor in the serum of women with primary breast cancer.Contemporary oncology (Poznan, Poland) · 2013Article
- Article
- Bone marrow stromal cells stimulate an angiogenic program that requires endothelial MT1-MMP.Journal of cellular physiology · 2012Article
- A flexible multidomain structure drives the function of the urokinase-type plasminogen activator receptor (uPAR).The Journal of biological chemistry · 2012Article
- Mimicry of the regulatory role of urokinase in lamellipodia formation by introduction of a non-native interdomain disulfide bond in its receptor.The Journal of biological chemistry · 2011Article
- Article
- Mesenchymal stem cells from adipose and bone marrow promote angiogenesis via distinct cytokine and protease expression mechanisms.Angiogenesis · 2011Article
- Article
- Mechanisms in the loss of capillaries in systemic sclerosis: angiogenesis versus vasculogenesis.Journal of cellular and molecular medicine · 2010Review
- Mesenchymal cells stimulate capillary morphogenesis via distinct proteolytic mechanisms.Experimental cell research · 2010Article
- Single and combined effects of alphavbeta3- and alpha5beta1-integrins on capillary tube formation in a human fibrinous matrix.Angiogenesis · 2009Article
- Thrombin bound to a fibrin clot confers angiogenic and haemostatic properties on endothelial progenitor cells.Journal of cellular and molecular medicine · 2008Article
- CD87 (urokinase-type plasminogen activator receptor), function and pathology in hematological disorders: a review.Leukemia · 2004Review
- Sustained expression of homeobox D10 inhibits angiogenesis.The American journal of pathology · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrin or a fibrinous exudate can facilitate angiogenesis in many pathological conditions. In vitro, the outgrowth of capillary-like structures in fibrin can be mimicked by exposing human microvascular endothelial cells (hMVECs) to an angiogenic growth factor and tumor necrosis factor (TNF)-alpha. Urokinase-type plasminogen activator (u-PA) and plasmin activities are required for this angiogenic process. This study focuses on the role and localization of the u-PA receptor (u-PAR) in newly formed microvascular structures. The u-PAR-blocking monoclonal antibody (MAb) H-2 completely inhibited the formation of capillary-like tubular structures induced by exposure of hMVECs to basic fibroblast growth factor and TNF-alpha. This was accompanied by a several-fold increase in u-PA accumulation in the conditioned medium. The effect of MAb H-2 was not caused by blocking cellular activation by u-PA/u-PAR interaction, as the amino-terminal fragment (ATF) of u-PA, which also activates u-PAR, prevented tube formation. In addition, the inhibition by MAb H-2 was not due to an effect of the antibody on u-PAR-vitronectin binding. These data show that inhibition of tube formation can be caused not only by inhibition of u-PA or plasmin activities but also by unavailability of the u-PAR for cell-bound proteolysis. Immunohistochemical analysis showed that in in vitro angiogenesis u-PAR and u-PA were localized on the invading, tube-forming hMVECs and not on the endothelial cells that are located on top of the fibrin matrix. u-PAR and u-PA were also prominently expressed on endothelial cells of neovessels present in an atherosclerotic plaque. These data may give more insight into the role of u-PAR in repair-associated angiogenesis.
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