Stressing Out Cells: flow-induced migration of endothelial cells and cell adhesion on hydrogels

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• Prof Gerry Fuller, University of Stanford
• Thursday 28 March 2013, 11:00-12:00
• Small Lecture Theatre, Cavendish Laboratory.

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Cells in the human body are constantly subjected to mechanical stresses and this lecture discusses two examples: the response of vascular endothelial cells to spatially inhomogeneous wall shear stresses and the adhesion of corneal epithelial cells to hydrogel surfaces (contact lenses).

The ability of the endothelial cells that line the interior of blood vessels to sense and respond to fluid flow is an essential component of cardiovascular development, homeostasis, and disease. In particular, the endothelium at arterial bends, branches, and at surface irregularities is prone to chronic inflammation that contributes to the development of atherosclerotic lesions. However, while extensive work has characterized the response of these cells to uniform, laminar flow, the response of endothelial cells to the complex, spatially varying wall shear stresses present in vivo remains poorly understood. We investigated the effects of complex flows on endothelial cells in vitro using a novel impinging flow device that exposes endothelial cells to shear stress gradients and stagnation point flows similar to those found at arterial bifurcations. We found that in all cases human microvascular endothelial cells migrated toward the vicinity of the stagnation point, and against the direction of fluid flow. We also found that these cells aligned parallel to the flow direction at low levels of shear stress, but perpendicular to the flow direction near the center, stagnation point. These observations suggest that endothelial cell migration and polarization may thus play presently unrecognized roles in the early stages of atherosclerotic lesion formation, particularly in regions of complex flow.

Adhesion of corneal epithelial cells to hydrogel surfaces causes discomfort when wearing contact lenses. Work is presented using a newly developed instrument where the stress-strain response of living cells sandwiched between two shearing surfaces can be measured. In these experiments, the moving, upper surface is a contact lens. Simultaneously, live-cell imaging is conducted to reveal cell deformation when adhesion to the lens occurs. It is demonstrated that cell-lens adhesion is greatly accelerated in the presence of lysozyme, a protein presence in the tear film. The influence of this protein on dewetting of contact lens surfaces is also discussed.

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