Rupture Forces among Human Blood Platelets at different Degrees of Activation

Abstract

Little is known about mechanics underlying the interaction among platelets during activation and aggregation. Although the strength of a blood thrombus has likely major biological importance, no previous study has measured directly the adhesion forces of single platelet-platelet interaction at different activation states. Here, we filled this void first, by minimizing surface mediated platelet-activation and second, by generating a strong adhesion force between a single platelet and an AFM cantilever, preventing early platelet detachment. We applied our setup to measure rupture forces between two platelets using different platelet activation states, and blockade of platelet receptors. The rupture force was found to increase proportionally to the degree of platelet activation, but reduced with blockade of specific platelet receptors. Quantification of single platelet-platelet interaction provides major perspectives for testing and improving biocompatibility of new materials; quantifying the effect of drugs on platelet function; and assessing the mechanical characteristics of acquired/inherited platelet defects.

PlA2 Polymorphism in Glycoprotein IIb/IIIa Modulates the Morphology and Nanomechanics of Platelets

“…26 Recently, atomic force microscopy (AFM) was applied to investigate the biomechanical characteristics and 3-dimensional changes in platelet architecture on activation. 2,3,6,29 The experiments on elasticity in parallel with depolymerization of cytoskeleton provided a new light on the cell biomechanics. 4 The aim of our study was to assess the changes in the topology and membrane elasticity (Young's modulus) of platelets isolated from healthy individuals and patients with deep venous thrombosis (DVT) at the cell spreading stage and to evaluate the impact of the carriage of allele PlA2 in GPIIb/IIIa on their nanomechanical properties.…”

“…1,2 Various factors, including inherited ones, control the platelet morphology and thereby cause alterations in their nanomechanical properties. [1][2][3][4][5][6] Resting platelets are nonadhesive anucleate 2 to 5 mm discoid cells, 1,7 possessing thick wrinkled membrane and circulating in the bloodstream. They respond to vasculature damage and shear stress by simultaneous shape changefirst they convert from compact discoid to asymmetrical spheres and then flatten and spread on the surface of damaged endothelium by extending actin-rich filopodia and lamellae.…”

Single‐molecule force spectroscopy applied to heparin‐induced thrombocytopenia

“…Recently, platelet‐surface activation has been investigated carefully by immobilizing them on glass coated with different materials such as collagens, fibronectin, and poly‐ l ‐lysine (PLL) . Because a set of SCFS experiment generally requires ~15 minutes to complete, platelet‐surface activation after 15 minutes settling on the surfaces was characterized.…”

“…The critical stiffness boundary between weak and strong platelet activation is ~5 kPa . In addition, platelets were also found to spread slower on soft collagen G coated glass and faster on the stiff surfaces coated with Horm collagen, fibronectin, or PLL . Dissimilar amount of platelet activating groups may also be the reason for slower platelet activation on collagen G as compared with Horm‐collagen or other materials .…”

Not Only Heparin but Also Antibody Induces Thrombocytopenia

“…The binding strength of a blood thrombus has major biological importance. A recent study could determine directly the binding strength between two platelets at single platelet level [13]. The binding force increases proportionally to the degree of platelet activation but reduces with blockade of specific platelet receptors.…”