ArticleArteriosclerosis, thrombosis, and vascular biology2011
Multifaceted role of plasminogen activator inhibitor-1 in regulating early remodeling of vein bypass grafts.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- PAI-1 Regulates the Cytoskeleton and Intrinsic Stiffness of Vascular Smooth Muscle Cells.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Oncostatin M, Serpins, and Oxidative Stress in Extracellular Matrix Remodeling and Arteriovenous Fistula Maturation.Cardiology and cardiovascular medicine · 2023Article
- Article
- Drug Targeting of Plasminogen Activator Inhibitor-1 Inhibits Metabolic Dysfunction and Atherosclerosis in a Murine Model of Metabolic Syndrome.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- S100B regulates inflammatory response during osteoarthritis via fibroblast growth factor receptor 1 signaling.Molecular medicine reports · 2018Article
- Long noncoding RNA RP4 functions as a competing endogenous RNA through miR-7-5p sponge activity in colorectal cancer.World journal of gastroenterology · 2018Article
- Inflammation in Vein Graft Disease.Frontiers in cardiovascular medicine · 2018Review
- Oxidized low density lipoprotein facilitates tumor necrosis factor‑α mediated chondrocyte death via autophagy pathway.Molecular medicine reports · 2017Article
- Plasminogen activator inhibitor-1 regulates the vascular expression of vitronectin.Journal of thrombosis and haemostasis : JTH · 2017Article
- Role of IL-17 in LPS-induced acute lung injury: anOncotarget · 2017Article
- Recombinant soluble apyrase APT102 inhibits thrombosis and intimal hyperplasia in vein grafts without adversely affecting hemostasis or re-endothelialization.Journal of thrombosis and haemostasis : JTH · 2017Article
- Upregulation of MiR-29b contributes to mesenchymal stem cell dysfunction in patients with severe pre-eclampsia.International journal of clinical and experimental pathology · 2017Article
- Pharmacological Targeting of Plasminogen Activator Inhibitor-1 Decreases Vascular Smooth Muscle Cell Migration and Neointima Formation.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- Vein graft failure: from pathophysiology to clinical outcomes.Nature reviews. Cardiology · 2016Review
- Platelets: Context-Dependent Vascular Protectors or Mediators of Disease.Arteriosclerosis, thrombosis, and vascular biology · 2015Review
- Plasminogen activator inhibitor-1 suppresses profibrotic responses in fibroblasts from fibrotic lungs.The Journal of biological chemistry · 2015Article
- C-reactive protein induces expression of tissue factor and plasminogen activator inhibitor-1 and promotes fibrin accumulation in vein grafts.Journal of thrombosis and haemostasis : JTH · 2014Article
- SENP3 regulates high glucose-induced endothelial dysfunction via ROS dependent signaling.Diabetes & vascular disease researchArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe role of plasminogen activator inhibitor-1 (PAI-1) in vein graft (VG) remodeling is undefined. We examined the effect of PAI-1 on VG intimal hyperplasia and tested the hypothesis that PAI-1 regulates VG thrombin activity. METHODS AND
resultsVGs from wild-type (WT), Pai1(-/-), and PAI-1-transgenic mice were implanted into WT, Pai1(-/-), or PAI-1-transgenic arteries. VG remodeling was assessed 4 weeks later. Intimal hyperplasia was significantly greater in PAI-1-deficient mice than in WT mice. The proliferative effect of PAI-1 deficiency was retained in vitronectin-deficient mice, suggesting that PAI-1's antiproteolytic function plays a key role in regulating intimal hyperplasia. Thrombin-induced proliferation of PAI-1-deficient venous smooth muscle cells (SMC) was significantly greater than that of WT SMC, and thrombin activity was significantly higher in PAI-1-deficient VGs than in WT VGs. Increased PAI-1 expression, which has been associated with obstructive VG disease, did not increase intimal hyperplasia.
conclusionsDecreased PAI-1 expression (1) promotes intimal hyperplasia by pathways that do not require vitronectin and (2) increases thrombin activity in VG. PAI-1 overexpression, although it promotes SMC migration in vitro, did not increase intimal hyperplasia. These results challenge the concept that PAI-1 drives nonthrombotic obstructive disease in VG and suggest that PAI-1's antiproteolytic function, including its antithrombin activity, inhibits intimal hyperplasia.
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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.