Affiliations: Department of Biomedical Engineering, Duke University, Durham, NC 27708, USA
Note: [] Address for correspondence: George A. Truskey, Ph.D., Department of Biomedical Engineering, Duke University, 136 Hudson Hall, Campus Box 90281, Durham, NC 27708‐0281, USA. Tel.: +1 919 660 5147; Fax: +1 919 660 5362; E‐mail: george.truskey@duke.edu.
Abstract: Adhesion of monocytes to arterial endothelium may contribute to the asymmetric distribution of atherosclerotic lesions. Possible mechanisms for adhesion in the relatively high shear stress environment found in arteries include greater monocyte deformation and/or more frequent penetration of microvilli through steric and charge barriers. In vivo, secondary flows generate forces acting normal to the endothelial cell surface. These forces may cause compression of the microvilli or enable cells to overcome steric or electrostatic barriers, increasing adhesion. To investigate this, we examined monocyte adhesion to activated endothelium in recirculating flow. Adhesion was characterized by short arrests in a narrow region on either side of the reattachment line. The median arrest time was longer than that observed at comparable shear stresses in a linear shear flow. The lifetimes of adhesion were analyzed using a model for multiple bond formation. For cells adhering near the reattachment line, the bond number per cell was greater than the value found for similar shear stresses under shear flow. Thus, multiple bond formation arising from greater normal forces in recirculating flow permits monocytes to adhere at higher shear stresses.
