Resolving Two-dimensional Kinetics of the Integrin αIIbβ3-Fibrinogen Interactions Using Binding-Unbinding Correlation Spectroscopy

Litvinov, Rustem I.; Mekler, Andrey; Shuman, Henry; Bennett, Joel S.; Barsegov, Valeri; Weisel, John W.

doi:10.1074/jbc.m112.404848

Cited by 40 publications

(52 citation statements)

References 45 publications

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“…However, we are applying very weak loading rates on each bond ($ 4:10 À2 À 4 pN/s), and rebinding might play a role. Litvinov et al (32) found much larger off rates for fibrinogen-integrin interactions than we did in this study, on the order of k 0 $ 1 s À1 . This large discrepancy with our value for k 0 could be a signature of the rebinding that we neglected in our model.…”

Section: Existence Of Intact Adhesion Area After Cell Detachmentcontrasting

confidence: 48%

Characterizing Cell Adhesion by Using Micropipette Aspiration

Hogan

Babataheri

Hwang

et al. 2015

Biophysical Journal

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We have developed a technique to directly quantify cell-substrate adhesion force using micropipette aspiration. The micropipette is positioned perpendicular to the surface of an adherent cell and a constant-rate aspiration pressure is applied. Since the micropipette diameter and the aspiration pressure are our control parameters, we have direct knowledge of the aspiration force, whereas the cell behavior is monitored either in brightfield or interference reflection microscopy. This setup thus allows us to explore a range of geometric parameters, such as projected cell area, adhesion area, or pipette size, as well as dynamical parameters such as the loading rate. We find that cell detachment is a well-defined event occurring at a critical aspiration pressure, and that the detachment force scales with the cell adhesion area (for a given micropipette diameter and loading rate), which defines a critical stress. Taking into account the cell adhesion area, intrinsic parameters of the adhesion bonds, and the loading rate, a minimal model provides an expression for the critical stress that helps rationalize our experimental results.

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Section: Existence Of Intact Adhesion Area After Cell Detachmentcontrasting

confidence: 48%

Characterizing Cell Adhesion by Using Micropipette Aspiration

Hogan

Babataheri

Hwang

et al. 2015

Biophysical Journal

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“…The apparent force-free kinetic rate for association (on-rate) kЈ on was obtained using the experimental value of the binding probability P b (T) measured at time T (interaction time), expressed in terms of k off and kЈ on by the following equation (26).…”

Section: Analysis Of the Kinetics Of Kko-and Rto-pf4mentioning

confidence: 99%

Distinct Specificity and Single-molecule Kinetics Characterize the Interaction of Pathogenic and Non-pathogenic Antibodies against Platelet Factor 4-Heparin Complexes with Platelet Factor 4

Litvinov¹,

Yarovoi

Rauova

et al. 2013

Journal of Biological Chemistry

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Background: Heparin-treated patients often develop antibodies, but only a subset cause heparin-induced thrombocytopenia. Results: In a single-molecule assay, a pathogenic monoclonal antibody bound more strongly to cross-linked platelet factor 4 than a non-pathogenic antibody. Conclusion: Oligomerization of platelet factor 4 may enhance binding of pathogenic antibodies. Significance: A molecular basis for specificity of pathogenic antibodies in heparin-induced thrombocytopenia is provided.

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“…22,35 Mn 11 enhances binding of aIIbb3 to fibrinogen by increasing the binding energy and by decreasing the off-rate for this interaction. 36 It is not known how Mn 11 effects the binding of aIIbb3…”

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confidence: 99%

Both platelet- and endothelial cell–derived ERp5 support thrombus formation in a laser-induced mouse model of thrombosis

Passam

Lin

Gopal

et al. 2015

Blood

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• ERp5, like its family members PDI and ERp57, accumulates at sites of vessel wall injury.• Both platelets and endothelium secrete ERp5 on activation and contribute ERp5 necessary for thrombus formation in vivo.Protein disulfide isomerase (PDI) and endoplasmic reticulum protein 57 (ERp57) are emerging as important regulators of thrombus formation. Another thiol isomerase, endoplasmic reticulum protein 5 (ERp5), is involved in platelet activation. We show here the involvement of ERp5 in thrombus formation using the mouse laser-injury model of thrombosis and a specific antibody raised against recombinant ERp5. Anti-ERp5 antibody inhibited ERp5-dependent platelet and endothelial cell disulfide reductase activity in vitro. ERp5 release at the thrombus site was detected after infusion of Alexa Fluor 488-labeled anti-ERp5 antibody at 0.05 mg/g body weight, a dose that does not inhibit thrombus formation. Anti-ERp5 at 3 mg/g body weight inhibited laser-induced thrombus formation in vivo by causing a 70% decrease in the deposition of platelets and a 62% decrease in fibrin accumulation compared to infusion of control antibody (P < .01). ERp5 binds to b3 integrin with an equilibrium dissociation constant (K D ) of 21 mM, measured by surface plasmon resonance. The cysteine residues in the ERp5 active sites are not required for binding to b3 integrin. These results provide evidence for a novel role of ERp5 in thrombus formation, a function that may be mediated through its association with aIIbb3.

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Resolving Two-dimensional Kinetics of the Integrin αIIbβ3-Fibrinogen Interactions Using Binding-Unbinding Correlation Spectroscopy

Cited by 40 publications

References 45 publications

Characterizing Cell Adhesion by Using Micropipette Aspiration

Characterizing Cell Adhesion by Using Micropipette Aspiration

Distinct Specificity and Single-molecule Kinetics Characterize the Interaction of Pathogenic and Non-pathogenic Antibodies against Platelet Factor 4-Heparin Complexes with Platelet Factor 4

Both platelet- and endothelial cell–derived ERp5 support thrombus formation in a laser-induced mouse model of thrombosis

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