ArticleArteriosclerosis, thrombosis, and vascular biology2013
4-Hydroxy-2-nonenal enhances tissue factor activity in human monocytic cells via p38 mitogen-activated protein kinase activation-dependent phosphatidylserine exposure.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Tissue factor-dependent colitogenic CD4Nature communications · 2025Article
- Membrane curvature and PS localize coagulation proteins to filopodia and retraction fibers of endothelial cells.Blood advances · 2023Article
- The role of monocytes in thrombotic diseases: a review.Frontiers in cardiovascular medicine · 2023Review
- Extracellular Vesicles in Redox Signaling and Metabolic Regulation in Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Involvement of 4-hydroxy-2-nonenal in the pathogenesis of pulmonary fibrosis.Molecular and cellular biochemistry · 2021Review
- Extracellular Vesicles under Oxidative Stress Conditions: Biological Properties and Physiological Roles.Cells · 2021Review
- Type 1 interferon aggravates lipopolysaccharide-induced sepsis through upregulating Caspase-11 and Gasdermin D.Journal of physiology and biochemistry · 2021Article
- New Cellular Source of TF (Tissue Factor)-Positive Extracellular Vesicles in the Circulation.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Oxidative Stress Product, 4-Hydroxy-2-Nonenal, Induces the Release of Tissue Factor-Positive Microvesicles From Perivascular Cells Into Circulation.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Proeryptotic Activity of 4-Hydroxynonenal: A New Potential Physiopathological Role for Lipid Peroxidation Products.Biomolecules · 2020Article
- The procoagulant activity of tissue factor expressed on fibroblasts is increased by tissue factor-negative extracellular vesicles.PloS one · 2020Article
- Role of flavonoids in thrombotic, cardiovascular, and inflammatory diseases.Inflammopharmacology · 2019Review
- Role of Cell Surface Lipids and Thiol-Disulphide Exchange Pathways in Regulating the Encryption and Decryption of Tissue Factor.Thrombosis and haemostasis · 2019Review
- Lipoxidation in cardiovascular diseases.Redox biology · 2019Review
- Redox-dependent thiol modifications: implications for the release of extracellular vesicles.Cellular and molecular life sciences : CMLS · 2018Review
- The Potential Roles of Extracellular Vesicles in Cigarette Smoke-Associated Diseases.Oxidative medicine and cellular longevity · 2018Review
- The lipid peroxidation product 4-hydroxy-2-nonenal induces tissue factor decryption via ROS generation and the thioredoxin system.Blood advances · 2017Article
- Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair.Redox biology · 2015Review
- Foam cell-derived 4-hydroxynonenal induces endothelial cell senescence in a TXNIP-dependent manner.Journal of cellular and molecular medicine · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objective4-hydroxy-2-nonenal (HNE) is one of the major aldehydes formed during lipid peroxidation and is believed to play a role in the pathogenesis of atherosclerosis. The objective of the present study is to investigate the effect of HNE on tissue factor (TF) procoagulant activity expressed on cell surfaces. APPROACH AND
resultsTF activity and antigen levels on intact cells were measured using factor Xa generation and TF monoclonal antibody binding assays, respectively. Exposure of phosphatidylserine on the cell surface was analyzed using thrombin generation assay or by binding of a fluorescent dye-conjugated annexin V. 2',7'-dichlorodihydrofluorescein diacetate was used to detect the generation of reactive oxygen species. Our data showed that HNE increased the procoagulant activity of unperturbed THP-1 cells that express traces of TF antigen, but had no effect on unperturbed endothelial cells that express no measurable TF antigen. HNE increased TF procoagulant activity but not TF antigen of both activated monocytic and endothelial cells. HNE treatment generated reactive oxygen species, activated p38 mitogen-activated protein kinase, and increased the exposure of phosphatidylserine at the outer leaflet in THP-1 cells. Treatment of THP-1 cells with an antioxidant, N-acetyl cysteine, suppressed the above HNE-induced responses and negated the HNE-mediated increase in TF activity. Blockade of p38 mitogen-activated protein kinase activation inhibited HNE-induced phosphatidylserine exposure and increased TF activity.
conclusionsHNE increases TF coagulant activity in monocytic cells through a novel mechanism involving p38 mitogen-activated protein kinase activation that leads to enhanced phosphatidylserine exposure at the cell surface.
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