Flow-mediated endothelial mechanotransduction. Macrorheology and adaptive microrheology of endothelial cells subjected to fluid shear stress. A mechanoelectrochemical model of radial deformation of the capillary glycocalyx. Role of deformable cancer cells on wall shear stress-associated-VEGF secretion by endothelium in microvasculature. The LDL transport across the deformable arterial wall: the effect of endothelial cell turnover and intimal deformation under hypertension. Shear induced force transmission in a multicomponent, multicell model of the endothelium. Mechanotransmission in endothelial cells subjected to oscillatory and multi-directional shear flow. Localization of rolling and firm-adhesive interactions between tumor cells and endothelium in microvasculature. Fluid shear stress on endothelial cells modulates mechanical tension across VE-cadherin and PECAM-1. Effects of extracellular matrix viscoelasticity on cellular behaviour. Effects of biaxial oscillatory shear stress on endothelial cell proliferation and morphology. Diffusion of clusters of transmembrane proteins as a model of focal adhesion remodeling. Force–extension relationship of cell–cell contacts. The asymmetric self-assembly mechanism of adherens junctions: a cellular push–pull unit. MSc Thesis, The Pennsylvania State University, Department of Bioengineering, 2007.īrevier, J., D. Multiscale finite element analysis of focal adhesion in sheared endothelial cells. Local measurements of viscoelastic parameters of adherent cell surfaces by magnetic bead microrheometry. Subcellular distribution of shear stress at the surface of flow-aligned and nonaligned endothelial monolayer. A model for shear stress-induced deformation of a flow sensor on the surface of vascular endothelial cells. Force and focal adhesion assembly: a close relationship studied using elastic micropatterned substrates. Atelectrauma disrupts pulmonary epithelial barrier integrity and alters the distribution of tight junction proteins ZO-1 and claudin 4. The identification of ECs mechanosensors involved in early stages of EC-cancer cell interaction will help with developing more efficient therapeutic interventions to suppress cancer cell transmigration in the microvasculature.Īnne-Marie, J., and P. This finding reveals the role of organ-specific stiffness in promoting cancer cell transmigration even in capillaries larger than cancer cell diameter.Ĭonclusions-ÊCancer cell-induced-changes in ECs mechanotransduction represents an important potential mechanism for cancer cell transmigration in the microvasculature particularly with stiffer ECM. Impact of ECM stiffness is particularly significant in ECs exposed to fluid shear stresses of 2 Pa or lower. Furthermore, we demonstrate that ADJs, FAs, and SFs experience higher stresses in ECs attached to stiffer ECM.

This impact is more drastic on stress fibers (SFs) both centrally located and peripheral ones. Results-Our results show that cancer cell-altered hemodynamics results in significantly high forces transmitted to subcellular organelles of ECs which are in vicinity of cancer cells.

Methods-A three-dimensional, multiscale, multicomponent, viscoelastic model of focally adhered ECs is developed to simulate the force transmission through ECs mechanosensors. The second objective of this study is to elucidate the role of ECM stiffness on mechanotransduction in ECs. However, it is still not well understood how ECM stiffness impacts ECs mechanosensors.

Moreover, extracellular matrix (ECM) stiffening has been shown to correlate with progression of most cancer types. The first objective of present study is to explore how cancer cell-induced changes in local hemodynamics can impact the forces experienced by intra/inter-cellular organelles of ECs that are believed to play important roles in mechanotransduction. On the other hand, cancer cells are shown to influence the local hemodynamics in their vicinity, in microvasculature. Introduction-Local hemodynamics impact the mechanotransduction in endothelial cells (ECs) lining the vascular network.

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