LDL Decreases the Membrane Compliance and Cell Adhesion of Endothelial Cells Under Fluid Shear Stress
- PDF / 526,613 Bytes
- 8 Pages / 593.972 x 792 pts Page_size
- 50 Downloads / 190 Views
DL Decreases the Membrane Compliance and Cell Adhesion of Endothelial Cells Under Fluid Shear Stress DANGHENG WEI,1,2 YONGPENG CHEN,2 CHAOJUN TANG,2 HUA HUANG,2 LUSHAN LIU,1 ZUO WANG,1,2 RUMING LI,2 and GUIXUE WANG2 1 Key Laboratory for Arteriosclerology of Hunan Province, The Institute of Cardiovascular Disease, University of South China, Hengyang 421001, China; and 2Key Laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education, Bioengineering College of Chongqing University, Chongqing 400030, China
(Received 31 July 2012; accepted 8 October 2012; published online 18 October 2012) Associate Editor Konstantinos Konstantopoulos oversaw the review of this article.
cells, smooth muscle cells (SMC), the arterial wall, and fluid shear stress. Clinical, genetic, and epidemiological studies have indicated that elevated plasma concentrations of low-density lipoproteins (LDL) constitute an important risk factor for the premature onset of atherosclerosis and ischemic heart disease.10,27 Furthermore, the accumulation, chemical modification, and residence time of LDL within the vessel wall influence the pathological progression of arterial lesions.12,35 Locally elevated concentrations of LDL in the arterial system were shown to initiate atherosclerotic plaque formation.7,36,38,39 Clinical studies have also demonstrated that reducing low density lipoprotein-cholesterol (LDL-C) levels can improve clinical outcomes, both in patients at risk of cardiovascular disease and in high-risk patients already presenting clinical symptoms.1,9 Under physiological conditions, the endothelium presents a surface with antithrombogenic properties mediated by a capacity to produce and release substances such as nitric oxide. In the past 20 yeas, the pathological mechanisms of LDL-induced ECs dysfunction on endothelial activation and the expression of cytokines/chemokines and adhesion molecules were paid most attention.31 Recently, renewed attention is being paid to ECs mechanical behaviours. Study showed that aortic ECs from hypercholesterolemic pigs were significantly stiffer than cells from healthy animals.3 Risk factors for atherosclerosis such as tumor necrosis factor-a (TNF-a) and C-reactive protein (CRP) induced EC dysfunction with alternating EC mechanical properties.18,20 In this study, we speculated that LDL might change EC mechanical properties, which contribute to the progression of endothelial dysfunction. The viscoelastic properties of cells are important in predicting cell deformation under mechanical loading
Abstract—Atherosclerosis is an inflammatory disease of large and medium sized arteriole walls that is precipitated by elevated levels of low-density lipoprotein (LDL) cholesterol in the blood. However, the mechanisms that lead to the initiation of atherosclerosis are not fully understood. In this study, endothelial cells (ECs) were incubated with LDL for 24 h, and then the lipid was detected with Oil Red O staining and cholesterol ester was assayed with high-performance liquid chromatography (
Data Loading...
