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    Multi-scale simulation of L-selectin–PSGL-1-dependent homotypic leukocyte binding and rupture

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    https://link.springer.com/article/10.1007%2Fs10237-010-0201-2
    Permanent Link
    10.1007/s10237-010-0201-2
    http://hdl.handle.net/11603/11630
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    • UMBC Faculty Collection
    • UMBC Mechanical Engineering Department
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    Author/Creator
    Gupta, V.K.
    Sraj, Ihab A.
    Konstantopoulos, Konstantinos
    Eggleton, Charles D.
    Date
    2010-03-14
    Type of Work
    15 pages
    Text
    journal article
    Citation of Original Publication
    V. K. Gupta, Ihab A. Sraj, Konstantinos Konstantopoulos, Charles D. Eggleton, Multi-scale simulation of L-selectin–PSGL-1-dependent homotypic leukocyte binding and rupture, Biomechanics and Modeling in Mechanobiology October 2010, Volume 9, Issue 5, pp 613–627 , DOI 10.1007/s10237-010-0201-2
    Rights
    This item is likely protected under Title 17 of the U.S. Copyright Law. Unless on a Creative Commons license, for uses protected by Copyright Law, contact the copyright holder or the author.
    Subjects
    Cell adhesion
    Cell deformation
    Immersed boundary method
    Monte Carlo simulation
    Receptor–ligand bond kinetics
    UMBC High Performance Computing Facility (HPCF)
    Abstract
    L-selectin–PSGL-1-mediated polymorphonuclear (PMN) leukocyte homotypic interactions potentiate the extent of PMN recruitment to endothelial sites of inflammation. Cell–cell adhesion is a complex phenomenon involving the interplay of bond kinetics and hydrodynamics. As a first step, a 3-D computational model based on the Immersed Boundary Method is developed to simulate adhesion-detachment of two PMN cells in quiescent conditions. Our simulations predict that the total number of bonds formed is dictated by the number of available receptors (PSGL-1) when ligands (L-selectin) are in excess, while the excess amount of ligands influences the rate of bond formation. Increasing equilibrium bond length results in a higher number of receptor–ligand bonds due to an increased intercellular contact area. On-rate constants determine the rate of bond formation, while off-rates control the average number of bonds by modulating bond lifetimes. Application of an external pulling force leads to time-dependent on- and off-rates and causes bond rupture. Moreover, the time required for bond rupture in response to an external force is inversely proportional to the applied load and decreases with increasing off-rate.


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    Albin O. Kuhn Library & Gallery
    University of Maryland, Baltimore County
    1000 Hilltop Circle
    Baltimore, MD 21250
    www.umbc.edu/scholarworks

    Contact information:
    Email: scholarworks-group@umbc.edu
    Phone: 410-455-3544


    If you wish to submit a copyright complaint or withdrawal request, please email mdsoar-help@umd.edu.