Mechanisms for Flow-Enhanced Cell Adhesion

Zhu, Cheng; Yago, Tadayuki; Lou, Jizhong; Zarnitsyna, Veronika I.; McEver, Rodger P.

doi:10.1007/s10439-008-9464-5

Cited by 100 publications

(99 citation statements)

References 21 publications

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“…Platelet Rolling Velocities on 1238-A1, 1261-A1, and VWF Were Governed by Their Respective Slip-Catch-Slip, Slip-only, and Catch-Slip Bonds with GPIb␣-Previously, we demonstrated an inverse relationship between rolling velocity and bond lifetime-the longer the bond lifetime, the slower the rolling velocity (6, 39)-that provided definitive evidence that flowenhanced rolling is caused by catch bonds (40). To corroborate the single-bond lifetime results in Fig.…”

Section: Gpib␣ Dissociates From 1238-a1 As a Triphasic Slip-catchslipmentioning

confidence: 63%

The N-terminal Flanking Region of the A1 Domain Regulates the Force-dependent Binding of von Willebrand Factor to Platelet Glycoprotein Ibα

Ju¹,

Dong

Crúz

et al. 2013

Journal of Biological Chemistry

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193

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Section: Gpib␣ Dissociates From 1238-a1 As a Triphasic Slip-catchslipmentioning

confidence: 63%

The N-terminal Flanking Region of the A1 Domain Regulates the Force-dependent Binding of von Willebrand Factor to Platelet Glycoprotein Ibα

Ju¹,

Dong

Crúz

et al. 2013

Journal of Biological Chemistry

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193

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“…L-selectin is expressed on leukocytes and binds to P-selectin glycoprotein ligand-1 (PSGL-1), 4 a leukocyte mucin, and to 6-sulfo-sialyl Lewis X (6-sulfo-sLe x ), a terminal component of glycans on a group of mucins expressed on endothelial cells in lymph nodes and some sites of inflammation (1). Selectin-ligand interactions provide adhesive forces for leukocytes to balance hemodynamic forces, and their kinetics have long been shown to depend on blood flow (2).…”

mentioning

confidence: 99%

Regulation of Catch Bonds by Rate of Force Application

Sarangapani¹,

Qian²,

Chen

et al. 2011

Journal of Biological Chemistry

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The current paradigm for receptor-ligand dissociation kinetics assumes off-rates as functions of instantaneous force without impact from its prior history. This a priori assumption is the foundation for predicting dissociation from a given initial state using kinetic equations. Here we have invalidated this assumption by demonstrating the impact of force history with singlebond kinetic experiments involving selectins and their ligands that mediate leukocyte tethering and rolling on vascular surfaces during inflammation. Dissociation of bonds between L-selectin and P-selectin glycoprotein ligand-1 (PSGL-1) loaded at a constant ramp rate to a constant hold force behaved as catchslip bonds at low ramp rates that transformed to slip-only bonds at high ramp rates. Strikingly, bonds between L-selectin and 6-sulfo-sialyl Lewis X were impervious to ramp rate changes. This ligand-specific force history effect resembled the effect of a point mutation at the L-selectin surface (L-selectinA108H) predicted to contact the former but not the latter ligand, suggesting that the high ramp rate induced similar structural changes as the mutation. Although the A108H substitution in L-selectin eliminated the ramp rate responsiveness of its dissociation from PSGL-1, the inverse mutation H108A in P-selectin acquired the ramp rate responsiveness. Our data are well explained by the sliding-rebinding model for catch-slip bonds extended to incorporate the additional force history dependence, with Ala-108 playing a pivotal role in this structural mechanism. These results call for a paradigm shift in modeling the mechanical regulation of receptor-ligand bond dissociation, which includes conformational coupling between binding pocket and remote regions of the interacting molecules.Receptor-ligand interactions are usually modeled by chemical reaction kinetics wherein force-dependent kinetic rates are key parameters (1). A typical example is the interactions between selectins and their ligands that mediate the tethering and rolling of circulating leukocytes on vascular surfaces during their recruitment to secondary lymphoid organs or inflammation sites (1). L-selectin is expressed on leukocytes and binds to P-selectin glycoprotein ligand-1 (PSGL-1), 4 a leukocyte mucin, and to 6-sulfo-sialyl Lewis X (6-sulfo-sLe x ), a terminal component of glycans on a group of mucins expressed on endothelial cells in lymph nodes and some sites of inflammation (1). Selectin-ligand interactions provide adhesive forces for leukocytes to balance hemodynamic forces, and their kinetics have long been shown to depend on blood flow (2).Since first modeled by Bell (3) and later by many others (4 -11), the existing paradigm for the mechanical regulation of receptor-ligand dissociation assumes a priori that the kinetic rates depend only on the instantaneous, present level of force on the bond but not its prior history. A simple model is the first-order single-step irreversible dissociation of single monomeric bonds:where p is the probability of having a bond at time t. ...

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“…Although a rate-controlled model of rolling adhesion does account for observed changes in adherent cell flux to a surface above and below the shear threshold, it does not provide a satisfactory explanation for why rolling cells in continuous contact with the surface roll progressively slower as the optimal level of fluid shear is approached. Rather, the favored hypothesis for the shear threshold postulates that the fluid force, translated through molecular linkages, regulates the lifetime and stability of adhesive contacts at the trailing edge of the rolling cell (6,11).…”

mentioning

confidence: 99%

Selectin catch–slip kinetics encode shear threshold adhesive behavior of rolling leukocytes

Beste¹,

Hammer

2008

Proc. Natl. Acad. Sci. U.S.A.

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The selectin family of leukocyte adhesion receptors is principally recognized for mediating transient rolling interactions during the inflammatory response. Recent studies using ultrasensitive force probes to characterize the force-lifetime relationship between Pand L-selectin and their endogenous ligands have underscored the ability of increasing levels of force to initially extend the lifetime of these complexes before disrupting bond integrity. This so-called ''catch-slip'' transition has provided an appealing explanation for shear threshold phenomena in which increasing levels of shear stress stabilize leukocyte rolling under flow. We recently incorporated catch-slip kinetics into a mechanical model for cell adhesion and corroborated this hypothesis for neutrophils adhering via L-selectin. Here, using adhesive dynamics simulations, we demonstrate that biomembrane force probe measurements of various Pand L-selectin catch bonds faithfully predict differences in cell adhesion patterns that have been described extensively in vitro. Using phenomenological parameters to characterize the dominant features of molecular force spectra, we construct a generalized phase map that reveals that robust shear-threshold behavior is possible only when an applied force very efficiently stabilizes the bound receptor complex. This criteria explains why only a subset of selectin catch bonds exhibit a shear threshold and leads to a quantitative relationship that may be used to predict the magnitude of the shear threshold for families of catch-slip bonds directly from their force spectra. Collectively, our results extend the conceptual framework of adhesive dynamics as a means to translate complex single-molecule biophysics to macroscopic cell behavior.force spectroscopy ͉ inflammation ͉ nanomechanics B y associating with cognate ligands on apposed surfaces, selectins expressed inducibly on the endothelial lumen (Eand P-selectin) and constitutively on the microvillar tips of peripheral blood leukocytes (L-selectin) mediate cell tethering and rolling adhesion (1). Stable rolling through L-selectin requires a threshold level of fluid shear stress, an unexpected but important consequence that prevents homotypic aggregation and inappropriate adhesion in low-shear environments (2-4). Much attention has focused on the underlying molecular kinetics to understand this behavior, with particular emphasis on the role of convective transport (5-8) and the molecular response to mechanical strain (9, 10). Several studies have now firmly established that fluid shear rate controls the tethering rate at which cells initially adhere to the substrate (6-8). Although a rate-controlled model of rolling adhesion does account for observed changes in adherent cell flux to a surface above and below the shear threshold, it does not provide a satisfactory explanation for why rolling cells in continuous contact with the surface roll progressively slower as the optimal level of fluid shear is approached. Rather, the favored hypothesis for the shear threshold po...

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Mechanisms for Flow-Enhanced Cell Adhesion

Cited by 100 publications

References 21 publications

The N-terminal Flanking Region of the A1 Domain Regulates the Force-dependent Binding of von Willebrand Factor to Platelet Glycoprotein Ibα

The N-terminal Flanking Region of the A1 Domain Regulates the Force-dependent Binding of von Willebrand Factor to Platelet Glycoprotein Ibα

Regulation of Catch Bonds by Rate of Force Application

Selectin catch–slip kinetics encode shear threshold adhesive behavior of rolling leukocytes

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