LDL decreases the membrane compliance and cell adhesion of endothelial cells under fluid shear stress.
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 (HPLC). F-actin was examined by fluorescence microscopy and the viscoelasticity of ECs was investigated using the micropipette aspiration technique. Then, a parallel-plate flow chamber device was used to observe the adhesion and retention of ECs under shear stress. The results demonstrated that elevated LDL significantly increased the cellular lipid content and induced the rearrangement of cytoskeletal F-actin. The initial rapid deformability (l/K 1 + l/K 2) was reduced by elevated cellular LDL levels, while membrane viscosity (μ) was increased by LDL accumulation. After treatment with 150 mg L(-1) LDL for 24 h, the adhesion of ECs under fluid shear stress was significantly decreased (p < 0.05). These results suggested that LDL induced cellular lipid accumulation and cytoskeleton reorganization which increased the cellular stiffness and decreased the adhesion of ECs.
Key Laboratory for Arteriosclerology of Hunan Province, The Institute of Cardiovascular Disease, University of South China, Hengyang, 421001, China.
Dangheng
D
Wei
Yongpeng
Y
Chen
Chaojun
C
Tang
Hua
H
Huang
Lushan
L
Liu
Zuo
Z
Wang
Ruming
R
Li
Guixue
G
Wang
D000199:Actins / Q000378:metabolism; D050197:Atherosclerosis / Q000209:etiology; D001696:Biomechanical Phenomena; D001698:Biomedical Engineering; D002448:Cell Adhesion / Q000502:physiology; D004548:Elasticity / Q000502:physiology; D042783:Endothelial Cells / Q000502:physiology*; D061307:Human Umbilical Vein Endothelial Cells; D006801:Humans; D050356:Lipid Metabolism; D008077:Lipoproteins, LDL / Q000502:physiology*; D013314:Stress, Mechanical; D014783:Viscosity
D000199:Actins; D008077:Lipoproteins, LDL