Bulletin of the American Physical Society
APS March Meeting 2010
Volume 55, Number 2
Monday–Friday, March 15–19, 2010; Portland, Oregon
Session L6: Intracellular Fluid Dynamics |
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Sponsoring Units: DFD Chair: Juan Del Alamo, University of California, San Diego Room: Portland Ballroom 253 |
Tuesday, March 16, 2010 2:30PM - 3:06PM |
L6.00001: Cell Quakes: Mechanics and Microrheology of Living Cells and Active Gels Invited Speaker: Recent experiments on molecular motor driven in vitro F-Actin networks have found anomalously large strain fluctuations at low frequency. In addition, the shear modulus of these active networks becomes as much as one hundred times larger than that of the same system in equilibrium. We develop a two-fluid mean-field model of a semiflexible network driven by molecular motors to explore these effects and show that, relying on only simple assumptions regarding the motor activity in the system, we can quantitatively understand both the low-frequency fluctuation enhancement and the nonequilibrium stiffening of the network. We discuss the implications of the fluctuation enhancement for intracellular microrheology. In particular we show that, by observing the anti-correlated motion of tracer particles in two-particle microrheology, one can calculate the density of active motor complexes and quantitatively account for these nonequilibrium forces in the analysis of the fluctuation data. Finally, we present the results of numerical work on the motor-induced gel stiffening effect in the high motor density limit, which goes beyond the analytic mean-field model. These results have implications for the interpretation of microrheology in such active networks including the cytoskeleton of living cells. In addition, they may form the basis for theoretical studies of biomimetic nonequilibrium gels whose mechanical properties are tunable through the control of their nonequilibrium steady state. [Preview Abstract] |
Tuesday, March 16, 2010 3:06PM - 3:42PM |
L6.00002: Intracellular Fluid Dynamics. Invited Speaker: |
Tuesday, March 16, 2010 3:42PM - 4:18PM |
L6.00003: Making the right choice: Biomechanical design making in tumor invasion Invited Speaker: Little is known about the complex interplay between the extracellular mechanical environment and the mechanical properties that characterize the intracellular environment during various stages of tumor metastasis. To date, most studies have focused on artificial 2D environments that are unrealistic and far from in vivo. In order to elucidate the cell-matrix relationship in cancer progression, we probe the intracellular and extra-cellular mechanical and biochemical environments to understand how tumor cells navigate the complex 3D environments. We simultaneously focus on cytoskeletal mechanics and intracellular signaling pathways as a function of dynamic matrix environments. Our results a non-linear dependence of focal adhesion protein (FAK) phosphorylation on matrix cross-linking and matrix mechanics. Increase in FAK phosphorylation is associated with actin cross-linking, changes in cell morphology and increased production of matrix degrading enzymes or MMPs. This production, in turn, affects adhesion through another feedback mechanism where MMPs regulate integrin expression and hence control cell shape, attachment and migration. Together, these two competing mechanisms control how cells respond to mechano-chemical changes in their local environment during single and collective migration in natural 3D environments. Our results highlight the interconnectivity of mechanical and chemical processes during 3D tumor invasion and identify key controllers of the cell decision process during tumor invasion. [Preview Abstract] |
Tuesday, March 16, 2010 4:18PM - 4:54PM |
L6.00004: Intracellular Fluid Dynamics. Invited Speaker: |
Tuesday, March 16, 2010 4:54PM - 5:30PM |
L6.00005: Anisotropic viscoelastic properties and cytoskeletal structure of endothelial cells subject to shear flow Invited Speaker: The cytoskeleton of adherent cells remodels in response to mechanical stimuli leading to a redistribution of intracellular forces that modifies cell function. We have analyzed the magnitude and anisotropy of the viscoelastic properties confluent vascular endothelial cells subject to continuous flow. For this purpose we used Directional Particle Tracking Microrheology, which measures the second-order tensor of intracellular marker displacements, allowing us to determine the principal directions of highest and lowest shear modulus at each position. We studied the orientation of these principal directions relative to the actin stress fibers. Before starting the flow, the cells' average cytoskeletal organization and shear modulus are isotropic. After the application of flow shear the cells' stress fibers gradually orient parallel to the flow and the principal directions of the shear modulus become parallel and perpendicular to the flow. The role of ATP-driven myosin-II contractions in the observed anisotropy is analyzed by using cells treated with drugs inhibiting myosin-II function. [Preview Abstract] |
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