dc.contributor.author | Gupta, V.K. | |
dc.contributor.author | Sraj, Ihab A. | |
dc.contributor.author | Konstantopoulos, Konstantinos | |
dc.contributor.author | Eggleton, Charles D. | |
dc.date.accessioned | 2018-10-22T13:37:55Z | |
dc.date.available | 2018-10-22T13:37:55Z | |
dc.date.issued | 2010-03-14 | |
dc.description.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. | en_US |
dc.description.sponsorship | The authorswould like to acknowledge the financial support provided by the National Institute of Health Grant RO1 AI063366. | en_US |
dc.description.uri | https://link.springer.com/article/10.1007%2Fs10237-010-0201-2 | en_US |
dc.format.extent | 15 pages | en_US |
dc.genre | journal article | en_US |
dc.identifier | doi:10.13016/M2B27PV7Z | |
dc.identifier.citation | 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 | en_US |
dc.identifier.uri | 10.1007/s10237-010-0201-2 | |
dc.identifier.uri | http://hdl.handle.net/11603/11630 | |
dc.language.iso | en_US | en_US |
dc.publisher | Springer-Verlag | en_US |
dc.relation.isAvailableAt | The University of Maryland, Baltimore County (UMBC) | |
dc.relation.ispartof | UMBC Mechanical Engineering Department Collection | |
dc.relation.ispartof | UMBC Faculty Collection | |
dc.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. | |
dc.subject | Cell adhesion | en_US |
dc.subject | Cell deformation | en_US |
dc.subject | Immersed boundary method | en_US |
dc.subject | Monte Carlo simulation | en_US |
dc.subject | Receptor–ligand bond kinetics | en_US |
dc.subject | UMBC High Performance Computing Facility (HPCF) | en_US |
dc.title | Multi-scale simulation of L-selectin–PSGL-1-dependent homotypic leukocyte binding and rupture | en_US |
dc.type | Text | en_US |