Effects of shear stress on the number and function of endothelial progenitor cells adhered to specific matrices
ABSTRACT The aim of this study was to screen specific adherent matrix for endothelial progenitor cells (EPCs), which can be used for antibody capturing stents.
In this study, the adhesion of EPCs on different matrices containing three different antibodies, VEGFR-2, CD34, CD133, was observed under shear stress in a flow chamber. Nitric oxide (NO) release, cell proliferation and the retention rate of EPCs, were measured separately.
The results demonstrated that shear stress within a certain range can promote proliferation and NO secretion of EPCs. Under the same shear stress, the EPCs showed stronger adhesion on matrix-containing CD133 antibody than on the other matrices.
CD133 antibody has the potential application for EPCs capture.
- [Show abstract] [Hide abstract]
ABSTRACT: Endothelial progenitor cells (EPCs) are a unique cell type found circulating in the peripheral blood with the capacity to become mature endothelial cells. EPCs can be released from many sources including the bone marrow, adipose tissue, and the vessel wall. Currently, there are two main methods of isolating EPCs: 1) separation during in vitro cell culture by morphological properties/differences, such as time of outgrowth, or 2) cell sorting with specific markers . There still remains debate with respect to the optimal isolation and culturing procedures; however, there is a consensus regarding the therapeutic potential of EPCs as a cell source for regenerative medicine, including for both replacement and endogenous repair. EPCs can be used as an endothelial cell source for prosthetic vascular grafts. Endogenously, EPCs home to the site of endothelial injury through the following 3 steps: 1) activation where the EPCs are deployed from their resident site as a result of EPC-activation factors, 2) targeting to the area of interest, and 3) exertion of their influence at the desired site. Each of these steps is an area of intense study. Previous studies primarily investigated the behavior of adherent EPCs, but it is unclear how circulating EPCs change in response to their shear environment into a more endothelial phenotype as they home to the site of endothelial injury. Obi et al seek to answer this question in their study in this issue of AJP-Cell . Obi et al. exposed EPCs to a flow environment that had a steady, unidirectional shear (0.25-2.5 dynes/cm2). Obi et al.'s results show that shear primes the EPC to become a mature endothelial cell in transit to its worksite. These results provide insight into how immature, circulating EPCs differentiate in response to flow and could participate in vascular regeneration and repair (both natural and engineered).AJP Cell Physiology 07/2012; 303(6):C589-91. DOI:10.1152/ajpcell.00224.2012
- [Show abstract] [Hide abstract]
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 (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.Annals of Biomedical Engineering 10/2012; 41(3). DOI:10.1007/s10439-012-0677-2