ArticleArteriosclerosis, thrombosis, and vascular biology2010
Activation of protease-activated receptors 3 and 4 accelerates tissue factor-induced thrombin generation on the surface of vascular smooth muscle cells.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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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
9 citing papers in PubMed, 17 citations in OpenAlex.
- NF-κB-Mediated Upregulation of Tissue Factor Contributes to the Procoagulant Phenotype of Smooth Muscle Cells from Abdominal Aorta Aneurysm in Human.Thrombosis and haemostasis · 2026Article
- Intercellular synergy between protease-activated receptors 1 and 4 during mouse development.Journal of thrombosis and haemostasis : JTH · 2025Article
- Elevated protease-activated receptor 4 (PAR4) gene expression in Alzheimer's disease predicts cognitive decline.Neurobiology of aging · 2024Article
- Activation of Human Platelets byPathogens (Basel, Switzerland) · 2022Article
- Platelets differentially modulate CD4Immunologic research · 2022Article
- Protease-activated receptor 4: from structure to function and back again.British journal of pharmacology · 2016Review
- Article
- Thrombin and vascular inflammation.Molecular and cellular biochemistry · 2012Review
- Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveTo determine factors regulating human aortic smooth muscle cells (HASMC) supported tissue factor-induced thrombin generation. METHODS AND
resultsThe addition of nonlipidated tissue factor and Ca(2+) to HASMCs maintained in reptilase-treated platelet-poor plasma resulted in the robust formation of thrombin after a lag phase of approximately 6 minutes. Pretreatment with low concentrations of α-thrombin before the addition of tissue factor and Ca(2+) accelerated the rate of thrombin generation (time to reach half of peak thrombin was reduced by [mean ± SD] 42.0 ± 2.2%; P<0.05) but had no effect on the amount of peak thrombin generated. Protease-activated receptor (PAR) 3 activating peptides (APs) or PAR-4 APs accelerated thrombin generation without affecting peak thrombin levels (time to half of peak thrombin decreased by 17.4 ± 5.6% and 21.7 ± 3.5%; P<0.05 with PAR-3 AP and PAR-4 AP, respectively). The addition of PAR-3 AP and PAR-4 AP together had an additive effect, with a reduction in time to half of peak thrombin of 43.9 ± 4.0%. PAR-3 AP or PAR-4 AP enhanced tissue factor-induced factor Xa production and phosphatidylserine exposure on the surface of HASMCs. PAR-1 activation had no effect on thrombin generation, factor Xa production, or phosphatidylserine exposure.
conclusionsLow concentrations of α-thrombin accelerate tissue factor-induced thrombin generation on the surface of HASMCs, and this effect is mediated by PAR-3 and PAR-4.
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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.