ArticleJournal of thrombosis and haemostasis : JTH2010
Plasminogen activator inhibitor-1 and vitronectin expression level and stoichiometry regulate vascular smooth muscle cell migration through physiological collagen matrices.
Article in Journal of thrombosis and haemostasis : JTH, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Serum proteomics identify biomarkers and pathogenesis of portopulmonary hypertension diagnosed based on echocardiography.Scientific reports · 2025Article
- "Super" SERPINs-A stabilizing force against fibrinolysis in thromboinflammatory conditions.Frontiers in cardiovascular medicine · 2023Review
- Correlations between vitronectin, miR-520, and miR-34 in patients with stenosis of coronary arteries.Molecular biology reports · 2021Article
- Article
- Identification ofCancers · 2019Article
- Pancreatic stellate cells activated by mutant KRAS-mediated PAI-1 upregulation foster pancreatic cancer progression via IL-8.Theranostics · 2019Article
- Association between plasminogen activator inhibitor-1 and cardiovascular events: a systematic review and meta-analysis.Thrombosis journal · 2018Article
- Plasminogen activator inhibitor-1 regulates the vascular expression of vitronectin.Journal of thrombosis and haemostasis : JTH · 2017Article
- Resolving distinct molecular origins for copper effects on PAI-1.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2017Article
- Pharmacological Targeting of Plasminogen Activator Inhibitor-1 Decreases Vascular Smooth Muscle Cell Migration and Neointima Formation.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- TGF-β1-induced PAI-1 contributes to a profibrotic network in patients with eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2016Article
- Distinct encounter complexes of PAI-1 with plasminogen activators and vitronectin revealed by changes in the conformation and dynamics of the reactive center loop.Protein science : a publication of the Protein Society · 2016Article
- Activation of the D4 dopamine receptor attenuates proliferation and migration of vascular smooth muscle cells through downregulation of AT1a receptor expression.Hypertension research : official journal of the Japanese Society of Hypertension · 2015Article
- Chemical Antagonists of Plasminogen Activator Inhibitor-1: Mechanisms of Action and Therapeutic Potential in Vascular Disease.Journal of molecular and genetic medicine : an international journal of biomedical research · 2014Article
- Functionally stable plasminogen activator inhibitor-1 in a family with cardiovascular disease and vitiligo.Journal of thrombosis and thrombolysis · 2014Article
- Dopamine D₄ receptors inhibit proliferation and migration of vascular smooth muscle cells induced by insulin via down-regulation of insulin receptor expression.Cardiovascular diabetology · 2014Article
- SERPINE1 expression discriminates site-specific metastasis in human melanoma.Experimental dermatology · 2012Article
- Plasminogen activator inhibitor type 1 regulates microglial motility and phagocytic activity.Journal of neuroinflammation · 2012Article
- Complex Regulation of the Pericellular Proteolytic Microenvironment during Tumor Progression and Wound Repair: Functional Interactions between the Serine Protease and Matrix Metalloproteinase Cascades.Biochemistry research international · 2012Article
- Multifaceted role of plasminogen activator inhibitor-1 in regulating early remodeling of vein bypass grafts.Arteriosclerosis, thrombosis, and vascular biology · 2011Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundVascular smooth muscle cell (VSMC) migration is a critical process in arterial remodeling. Purified plasminogen activator inhibitor-1 (PAI-1) is reported to both promote and inhibit VSMC migration on two-dimensional (D) surfaces.
objectiveTo determine the effects of PAI-1 and vitronectin (VN) expressed by VSMC themselves on migration through physiological collagen matrices.
methodsWe studied migration of wild-type (WT), PAI-1-deficient, VN-deficient, PAI-1/VN doubly-deficient (DKO) and PAI-1-transgenic (Tg) VSMC through three-D collagen gels.
resultsWT VSMC migrated significantly slower than PAI-1- and VN-deficient VSMC, but significantly faster than DKO VSMC. Experiments with recombinant PAI-1 suggested that basal VSMC PAI-1 expression inhibits migration by binding VN, which is secreted by VSMC and binds collagen. However, PAI-1-over-expressing Tg VSMC migrated faster than WT VSMC. Reconstitution experiments with recombinant PAI-1 mutants suggested that the pro-migratory effect of PAI-1 over-expression required its anti-plasminogen activator (PA) and LDL receptor-related protein (LRP) binding functions, but not VN binding. While promoting VSMC migration in the absence of PAI-1, VN inhibited the pro-migratory effect of active PAI-1.
conclusionsIn isolation, VN and PAI-1 are each pro-migratory. However, via formation of a high-affinity, non-motogenic complex, PAI-1 and VN each buffers the other's pro-migratory effect. The level of PAI-1 expression by VSMC and the concentration of VN in extracellular matrix are critical determinants of whether PAI-1 and VN promote or inhibit migration. These findings help to rectify previously conflicting reports and suggest that PAI-1/VN stoichiometry plays an important role in VSMC migration and vascular remodeling.
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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.