ArticleJournal of thrombosis and haemostasis : JTH2014
Plasminogen activator-1 overexpression decreases experimental postthrombotic vein wall fibrosis by a non-vitronectin-dependent mechanism.
Article in Journal of thrombosis and haemostasis : JTH, 2014. 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, 39 citations in OpenAlex.
- Targeting α6β1 integrin signaling with pranlukast to modulate venous endothelium function and reduce post-thrombotic vein wall injury.Journal of vascular surgery. Venous and lymphatic disorders · 2026Article
- Review
- Targeting Fibrinolytic Inhibition for Venous Thromboembolism Treatment: Overview of an Emerging Therapeutic Approach.Circulation · 2024Review
- Time-dependent ultrastructural changes during venous thrombogenesis and thrombus resolution.Journal of thrombosis and haemostasis : JTH · 2024Article
- Monocyte/macrophage-mediated venous thrombus resolution.Frontiers in immunology · 2024Review
- Immune cell-mediated venous thrombus resolution.Research and practice in thrombosis and haemostasis · 2023Review
- Current challenges in the prevention and management of post-thrombotic syndrome-towards improved prevention.International journal of hematology · 2023Review
- Mechanisms of cancer-associated thrombosis.Research and practice in thrombosis and haemostasis · 2023Article
- Experimental venous thrombus resolution is driven by IL-6 mediated monocyte actions.Scientific reports · 2023Article
- Crosstalk between septic shock and venous thromboembolism: a bioinformatics and immunoassay analysis.Frontiers in cellular and infection microbiology · 2023Article
- Modulation of interleukin-6 and its effect on late vein wall injury in a stasis mouse model of deep vein thrombosis.JVS-vascular science · 2022Article
- Plasminogen activator inhibitor 1 and venous thrombosis in pancreatic cancer.Blood advances · 2021Article
- Insights from experimental post-thrombotic syndrome and potential for novel therapies.Translational research : the journal of laboratory and clinical medicine · 2020Review
- Resolution of Deep Venous Thrombosis: Proposed Immune Paradigms.International journal of molecular sciences · 2020Review
- Genome-wide association analysis of venous thromboembolism identifies new risk loci and genetic overlap with arterial vascular disease.Nature genetics · 2019Article
- Fibrinolysis and Inflammation in Venous Thrombus Resolution.Frontiers in immunology · 2019Review
- Serpins in Venous Thrombosis and Venous Thrombus Resolution.Methods in molecular biology (Clifton, N.J.) · 2018Article
- TGF-β1 in Vascular Wall Pathology: Unraveling Chronic Venous Insufficiency Pathophysiology.International journal of molecular sciences · 2017Review
- Endotoxaemia-augmented murine venous thrombosis is dependent on TLR-4 and ICAM-1, and potentiated by neutropenia.Thrombosis and haemostasis · 2017Article
- Libby amphibole-induced mesothelial cell autoantibodies bind to surface plasminogen and alter collagen matrix remodeling.Physiological reports · 2016Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundFactors associated with postthrombotic syndrome are known clinically, but the underlying cellular processes at the vein wall are not well delineated. Prior work suggests that vein wall damage does not correlate with thrombus resolution but rather with plasminogen activator-1 (PAI-1) and matrix metalloproteinase (MMP) activity.
objectiveWe hypothesized that PAI-1 would confer post venous thrombosis (VT) vein wall protection via a vitronectin (Vn)-dependent mechanism.
methodsA stasis model of VT was used with harvest over 2 weeks, in wild-type, Vn(-/-) , and PAI-1-overexpressing mice (PAI-1 Tg).
resultsPAI-1 Tg mice had larger VT at 6 and 14 days, compared to controls, but Vn(-/-) mice had no alteration of VT resolution. Gene deletion of Vn resulted in an increase in, rather than the expected decrease in, circulating PAI-1 activity. While both Vn(-/-) and PAI-1 Tg had attenuated intimal fibrosis, PAI-1 Tg had significantly less vein wall collagen and a compensatory increase in collagen III gene expression. Both Vn(-/-) and PAI-1 Tg vein wall had less monocyte chemotactic factor-1 and fewer macrophages (F4/80), with significantly less MMP-2 activity and decreased TIMP-1 antigen. Ex vivo assessment of transforming growth factor β-mediated fibrotic response showed that PAI-1 Tg vein walls had increased profibrotic gene expression (collagens I and III, MMP-2, and α-smooth muscle actin) compared with controls, opposite of the in vivo response.
conclusionsThe absence of Vn increases circulating PAI-1, which positively modulates vein wall fibrosis in a dose-dependent manner. Translationally, PAI-1 elevation may decrease vein wall damage after deep vein thrombosis, perhaps by decreasing macrophage-mediated activities.
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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.