ArticleThrombosis journal2008
A new method to determine tissue specific tissue factor thrombomodulin activities: endotoxin and particulate air pollution induced disbalance.
Article in Thrombosis journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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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Who cites it
4 citing papers in PubMed, 17 citations in OpenAlex.
- Cardiopulmonary and Immune Effects of Environmental Particulate Exposures.Physiology (Bethesda, Md.) · 2026Review
- Effects of Particulate Matter on Inflammation and Thrombosis: Past Evidence for Future Prevention.International journal of environmental research and public health · 2022Review
- The procoagulant effects of fine particulate matter in vivo.Particle and fibre toxicology · 2011Article
- The relationship of air pollution and surrogate markers of endothelial dysfunction in a population-based sample of children.BMC public health · 2011Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIncrease in tissue factor (TF) and loss in thrombomodulin (TM) antigen levels has been described in various inflammatory disorders. The functional consequences of such changes in antigen concentrations in the coagulation balance are, however, not known. This study was designed to assess the consequences of inflammation-driven organ specific functional properties of the procoagulant response.
methodsTissue specific procoagulant activity was assessed by adding tissue homogenate to normal human pool plasma and recording of the thrombin generation curve. The new technique was subsequently applied on two inflammation driven animal models: 1) mouse lipopolysaccharide (LPS) induced endotoxemia and 2) spontaneously hypertensive rats exposed to environmental air pollution (particulate matter (PM).
resultsAddition of lung tissue from untreated animals to human plasma suppressed the endogenous thrombin potential (ETP) (175 +/- 61 vs. 1437 +/- 112 nM.min for control). This inhibitory effect was due to TM, because a) it was absent in protein C deficient plasma and b) lungs from TMpro/pro mice allowed full thrombin generation (ETP: 1686 +/- 209 nM.min). The inhibitory effect of TM was lost after LPS administration to mice, which induced TF activity in lungs of C57Bl/6 mice as well as increased the ETP (941 +/- 523 vs. 194 +/- 159 nM.min for control). Another pro-inflammatory stimulus, PM dose-dependently increased TF in the lungs of spontaneously hypertensive rats at 4 and 48 hours after PM exposure. The ETP increased up to 48 hours at the highest concentration of PM (1441 +/- 289 nM.min vs. saline: 164 +/- 64 nM.min, p < 0.0001), suggesting a concentration- and time dependent reduction in TM activity.
conclusionInflammation associated procoagulant effects in tissues are dependent on variations in activity of the TF-TM balance. The application of these novel organ specific functional assays is a useful tool to monitor inflammation-driven shifts in the coagulation balance within animal or human tissues.
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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.