NDLI: 4-Hydroxy-2-Nonenal Enhances Tissue Factor Activity in Human Monocytic Cells via p38 Mitogen-Activated Protein Kinase Activation-Dependent Phosphatidylserine Exposure

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4-Hydroxy-2-Nonenal Enhances Tissue Factor Activity in Human Monocytic Cells via p38 Mitogen-Activated Protein Kinase Activation-Dependent Phosphatidylserine Exposure

Content Provider	Scilit
Author	Vatsyayan, Rit Kothari, Hema Pendurthi, Usha R. Rao, L. Vijaya Mohan
Copyright Year	2013
Description	Journal: Arteriosclerosis, thrombosis, and vascular biology Objective—: 4-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 Results—: TF 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. Conclusions—: HNE 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.
Related Links	https://www.ahajournals.org/doi/pdf/10.1161/ATVBAHA.113.300972 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3883589/pdf https://www.ahajournals.org/doi/reader/10.1161/ATVBAHA.113.300972
Ending Page	1611
Page Count	11
Starting Page	1601
ISSN	10795642
e-ISSN	15244636
DOI	10.1161/atvbaha.113.300972
Journal	Arteriosclerosis, thrombosis, and vascular biology
Issue Number	7
Volume Number	33
Language	English
Publisher	Ovid Technologies (Wolters Kluwer Health)
Publisher Date	2013-07-01
Access Restriction	Open
Subject Keyword	Journal: Arteriosclerosis, thrombosis, and vascular biology P38 Mitogen-activated Protein Kinase 4-hydroxy-2-nonenal
Content Type	Text
Resource Type	Article
Subject	Cardiology and Cardiovascular Medicine

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4-Hydroxy-2-Nonenal Enhances Tissue Factor Activity in Human Monocytic Cells via p38 Mitogen-Activated Protein Kinase Activation-Dependent Phosphatidylserine Exposure

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