Tissue factor activity is upregulated in human endothelial cells exposed to oscillatory shear stress
Details
Serval ID
serval:BIB_791ECC5B2E39
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Tissue factor activity is upregulated in human endothelial cells exposed to oscillatory shear stress
Journal
Thrombosis and Haemostasis
ISSN
0340-6245 (Print)
Publication state
Published
Issued date
06/2002
Volume
87
Number
6
Pages
1062-8
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Jun
Research Support, Non-U.S. Gov't --- Old month value: Jun
Abstract
Hemodynamic forces play a critical role in the pathogenesis of atherosclerosis as evidenced by the focal nature of the disease. Oscillatory shear stress characterizes the hemodynamic environment of plaque-prone areas as opposed to unidirectional shear stress typical of plaque-free areas. These particular flow conditions modulate atherosclerosis-related genes. Tissue factor (TF) initiates blood coagulation, contributes to vascular remodeling, and is therefore a potential contributor in the development/progression of atherosclerosis. We investigated the effect of oscillatory and unidirectional flows on TF using an in vitro perfusion system. Human endothelial cells exposed for 24 h to oscillatory shear stress, significantly increased TF mRNA, and TF protein expression (1.5- and 1.75-fold, respectively, p < 0.01), and surface TF activity (twofolds-increase). Expression of TF inhibitor (TFPI), mRNA and protein, remained unchanged as compared to static conditions. Conversely, cells exposed to unidirectional shear, showed a decrease in TF activity with a significant increase in TFPI mRNA and protein expression (1.5- and 1.8-fold, respectively, p < 0.01). These results show for the first time that pulsatile oscillatory shear stress induces a pro-coagulant phenotype of endothelial cells which may favor formation/progression of atherothrombotic lesions.
Keywords
Apoptosis/physiology
Arteriosclerosis/etiology
Cell Line
Endothelium, Vascular/*metabolism
Equipment Design
Hemodynamic Processes/*physiology
Humans
Models, Cardiovascular
Perfusion
Periodicity
Stress, Mechanical
Thromboplastin/*metabolism
Up-Regulation
Pubmed
Web of science
Create date
17/01/2008 17:38
Last modification date
20/08/2019 15:35