Tailoring the Trajectory of Cell Rolling with Cytotactic Surfaces

Langmuir ◽  
2011 ◽  
Vol 27 (24) ◽  
pp. 15345-15351 ◽  
Author(s):  
Collin Edington ◽  
Hironobu Murata ◽  
Richard Koepsel ◽  
Jill Andersen ◽  
Sungeun Eom ◽  
...  
Keyword(s):  
Cell Rolling

scholarly journals Mechanical force effect on the two-state equilibrium of the hyaluronan-binding domain of CD44 in cell rolling

2015 ◽  
Vol 112 (22) ◽  
pp. 6991-6996 ◽  
Author(s):  
Takashi Suzuki ◽  
Miho Suzuki ◽  
Shinji Ogino ◽  
Ryo Umemoto ◽  
Noritaka Nishida ◽  
...  
Keyword(s):  
Shear Stress ◽  
Conformational Change ◽  
Mechanical Force ◽  
Binding Domain ◽  
Terminal Region ◽  
Hematopoietic Progenitor Cell ◽  
High Shear ◽  
Cell Rolling ◽  
High Affinity ◽  
C Terminus

CD44 is the receptor for hyaluronan (HA) and mediates cell rolling under fluid shear stress. The HA-binding domain (HABD) of CD44 interconverts between a low-affinity, ordered (O) state and a high-affinity, partially disordered (PD) state, by the conformational change of the C-terminal region, which is connected to the plasma membrane. To examine the role of tensile force on CD44-mediated rolling, we used a cell-free rolling system, in which recombinant HABDs were attached to beads through a C-terminal or N-terminal tag. We found that the rolling behavior was stabilized only at high shear stress, when the HABD was attached through the C-terminal tag. In contrast, no difference was observed for the beads coated with HABD mutants that constitutively adopt either the O state or the PD state. Steered molecular dynamics simulations suggested that the force from the C terminus disrupts the interaction between the C-terminal region and the core of the domain, thus providing structural insights into how the mechanical force triggers the allosteric O-to-PD transition. Based on these results, we propose that the force applied from the C terminus enhances the HABD–HA interactions by inducing the conformational change to the high-affinity PD transition more rapidly, thereby enabling CD44 to mediate lymphocyte trafficking and hematopoietic progenitor cell homing under high-shear conditions.

scholarly journals Stem cell membrane engineering for cell rolling using peptide conjugation and tuning of cell–selectin interaction kinetics

Biomaterials ◽  
2012 ◽  
Vol 33 (20) ◽  
pp. 5004-5012 ◽  
Author(s):  
Hao Cheng ◽  
Marta Byrska-Bishop ◽  
Cathy T. Zhang ◽  
Christian J. Kastrup ◽  
Nathaniel S. Hwang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Membrane ◽  
Cell Rolling ◽  
Peptide Conjugation ◽  
Interaction Kinetics ◽  
Membrane Engineering

scholarly journals Roles of cell and microvillus deformation and receptor-ligand binding kinetics in cell rolling

2008 ◽  
Vol 295 (4) ◽  
pp. H1439-H1450 ◽  
Author(s):  
Parag Pawar ◽  
Sameer Jadhav ◽  
Charles D. Eggleton ◽  
Konstantinos Konstantopoulos
Keyword(s):  
Ligand Binding ◽  
Three Dimensional ◽  
Theoretical Models ◽  
Binding Kinetics ◽  
Cell Deformation ◽  
Receptor Ligand ◽  
Length Scales ◽  
Bond Behavior ◽  
Cell Rolling ◽  
Threshold Phenomenon

Polymorphonuclear leukocyte (PMN) recruitment to sites of inflammation is initiated by selectin-mediated PMN tethering and rolling on activated endothelium under flow. Cell rolling is modulated by bulk cell deformation (mesoscale), microvillus deformability (microscale), and receptor-ligand binding kinetics (nanoscale). Selectin-ligand bonds exhibit a catch-slip bond behavior, and their dissociation is governed not only by the force but also by the force history. Whereas previous theoretical models have studied the significance of these three “length scales” in isolation, how their interplay affects cell rolling has yet to be resolved. We therefore developed a three-dimensional computational model that integrates the aforementioned length scales to delineate their relative contributions to PMN rolling. Our simulations predict that the catch-slip bond behavior and to a lesser extent bulk cell deformation are responsible for the shear threshold phenomenon. Cells bearing deformable rather than rigid microvilli roll slower only at high P-selectin site densities and elevated levels of shear (≥400 s−1). The more compliant cells (membrance stiffness = 1.2 dyn/cm) rolled slower than cells with a membrane stiffness of 3.0 dyn/cm at shear rates >50 s−1. In summary, our model demonstrates that cell rolling over a ligand-coated surface is a highly coordinated process characterized by a complex interplay between forces acting on three distinct length scales.

Role of cytoskeleton and deformability in laminin-mediated cell rolling

Biorheology ◽  
1998 ◽  
Vol 35 (1) ◽  
pp. 37-51
Author(s):  
S Wu
Keyword(s):  
Cell Rolling

scholarly journals A Semianalytical Model to Study the Effect of Cortical Tension on Cell Rolling

2010 ◽  
Vol 99 (12) ◽  
pp. 3870-3879 ◽  
Author(s):  
Suman Bose ◽  
Sarit K. Das ◽  
Jeffrey M. Karp ◽  
Rohit Karnik
Keyword(s):  
Cortical Tension ◽  
Cell Rolling

Lipid raft adhesion receptors and Syk regulate selectin-dependent rolling under flow conditions

Blood ◽  
2006 ◽  
Vol 108 (10) ◽  
pp. 3352-3359 ◽  
Author(s):  
Claire Abbal ◽  
Martine Lambelet ◽  
Debora Bertaggia ◽  
Carole Gerbex ◽  
Manuel Martinez ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Lipid Rafts ◽  
Lipid Raft ◽  
Chelating Agents ◽  
Regulatory Mechanisms ◽  
Membrane Microdomains ◽  
Leukocyte Rolling ◽  
Flow Conditions ◽  
Cell Rolling ◽  
Pharmacologic Inhibitors

Abstract Selectins and their ligand P-selectin glycoprotein ligand-1 (PSGL-1) mediate leukocyte rolling along inflamed vessels. Cell rolling is modulated by selectin interactions with their ligands and by topographic requirements including L-selectin and PSGL-1 clustering on tips of leukocyte microvilli. Lipid rafts are cell membrane microdomains reported to function as signaling platforms. Here, we show that disruption of leukocyte lipid rafts with cholesterol chelating agents depleted raft-associated PSGL-1 and L-selectin and strongly reduced L-, P-, and E-selectin–dependent rolling. Cholesterol repletion reversed inhibition of cell rolling. Importantly, leukocyte rolling on P-selectin induced the recruitment of spleen tyrosine kinase (Syk), a tyrosine kinase associated to lipid raft PSGL-1. Furthermore, inhibition of Syk activity or expression, with pharmacologic inhibitors or by RNA interference, strongly reduced leukocyte rolling on P-selectin, but not on E-selectin or PSGL-1. These observations identify novel regulatory mechanisms of leukocyte rolling on selectins with a strong dependency on lipid raft integrity and Syk activity.

scholarly journals Suppression of Prostate Cancer Cell Rolling and Adhesion to Endothelium by 1α,25-Dihydroxyvitamin D3

2011 ◽  
Vol 178 (2) ◽  
pp. 872-880 ◽  
Author(s):  
Jong-Wei Hsu ◽  
Sayeda Yasmin-Karim ◽  
Michael R. King ◽  
Joel C. Wojciechowski ◽  
Deanne Mickelsen ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Dihydroxyvitamin D3 ◽  
Cell Rolling

scholarly journals PSGL-1 and E/P-selectins are essential for T-cell rolling in inflamed CNS microvessels but dispensable for initiation of EAE

2014 ◽  
Vol 44 (8) ◽  
pp. 2287-2294 ◽  
Author(s):  
Karthik Sathiyanadan ◽  
Caroline Coisne ◽  
Gaby Enzmann ◽  
Urban Deutsch ◽  
Britta Engelhardt
Keyword(s):  
T Cell ◽  
Cell Rolling

Cooperation between Lateral Ligand Mobility and Accessibility for Receptor Recognition in Selectin-Induced Cell Rolling†,#

Biochemistry ◽  
2002 ◽  
Vol 41 (14) ◽  
pp. 4704-4712 ◽  
Author(s):  
Udo Bakowsky ◽  
Gabriele Schumacher ◽  
Christian Gege ◽  
Richard R. Schmidt ◽  
Ulrich Rothe ◽  
...  
Keyword(s):  
Cell Rolling ◽  
Receptor Recognition
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