Ai. Barakat, A model for shear stress-induced deformation of a flow sensor on the surface of vascular endothelial cells, J THEOR BIO, 210(2), 2001, pp. 221-236
Fluid mechanical shear stress elicits humoral, metabolic, and structural re
sponses in vascular endothelial cells (ECs); however, the mechanisms involv
ed in shear stress sensing and transduction remain incompletely understood.
Beyond being responsive to shear stress, ECs distinguish among and respond
differently to different types of shear stress. Recent observations sugges
t that endothelial shear stress sensing may occur through direct;interactio
n of the flow with cell-surface structures that act as primary Row sensors.
This paper presents a mathematical model for the shear stress-induced defo
rmation of a Row sensor on the EC surface. The sensor is modeled as a cytos
keleton-coupled viscoelastic structure exhibiting standard linear solid beh
avior. Since ECs respond differently to different types of flow, the deform
ation and resulting velocity of the sensor in response to steady, non-rever
sing pulsatile, and oscillatory Row have been studied. Furthermore, the sen
sitivity of the results to changes in various model parameters including th
e magnitude of applied shear stress, the constants that characterize the vi
scoelastic behavior, and the pulsatile flow frequency (f) has been investig
ated. The results have demonstrated that in response to a suddenly applied
shear stress, the sensor exhibits a level of instantaneous deformation foll
owed by gradual creeping to the long-term response. The peak deformation in
creases linearly with the magnitude of the applied shear stress and decreas
es for viscoelastic constants that correspond to stiffer sensors. While the
sensor deformation depends on f for low f values, the deformation becomes
f-independent above a critical threshold frequency. Finally, the peak senso
r deformation is considerably larger for steady and non-reversing pulsatile
flow than for oscillatory Row. If the extent of sensor deformation correla
tes with the intensity of flow-mediated endothelial signaling, then our res
ults suggest possible mechanisms by which ECs distinguish among steady, non
reversing pulsatile, and oscillatory shear stress. (C) 2001 Academic Press.