Imaging Molecular Adhesion in Cell Rolling by Adhesion Footprint Assay

Author(s):  
Scott Minh An ◽  
Seong Ho Kim ◽  
Vanessa J. White ◽  
Adam B. Yasunaga ◽  
Kathleen M. McMahon ◽  
...  



2015 ◽  
Vol 112 (22) ◽  
pp. 6991-6996 ◽  
Author(s):  
Takashi Suzuki ◽  
Miho Suzuki ◽  
Shinji Ogino ◽  
Ryo Umemoto ◽  
Noritaka Nishida ◽  
...  

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.



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


Biomaterials ◽  
2012 ◽  
Vol 33 (20) ◽  
pp. 5004-5012 ◽  
Author(s):  
Hao Cheng ◽  
Marta Byrska-Bishop ◽  
Cathy T. Zhang ◽  
Christian J. Kastrup ◽  
Nathaniel S. Hwang ◽  
...  


2021 ◽  
pp. 151015
Author(s):  
Dominik Dworschak ◽  
Carina Brunnhofer ◽  
Markus Valtiner
Keyword(s):  






2008 ◽  
Vol 295 (4) ◽  
pp. H1439-H1450 ◽  
Author(s):  
Parag Pawar ◽  
Sameer Jadhav ◽  
Charles D. Eggleton ◽  
Konstantinos Konstantopoulos

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.



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


2005 ◽  
Vol 22 (3) ◽  
pp. 229-240 ◽  
Author(s):  
Despina Bazou ◽  
George A. Foster ◽  
James R. Ralphs ◽  
W. Terence Coakley


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