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Platelet-surface interactions: priming of platelets by upstream agonists for downstream adhesion

Fig 1. A thiol to sulfonate surface gradient was generated by UV oxidation of surface thiols, then exposed to 10% platelet free plasma, followed by the washed platelet perfusion through two identical flow channels but in opposite directions. Adsorbed fibrinogen on the -SH side of the gradient primed platelets for the adhesion to the sulfonate end of the gradient downstream (panel B), however, this effect was absent whan the flow direction was reversed. (from Corum and Hlady, Biomaterials 31 (2010) 3148–3155).


Fig 2. Flow cell used in upstream- downstream studies (width = 0.5 cm, height = 0.025 cm, wall shear rate, = 100 1/s). Flow of platelets (5 min @ 20 ml/h) leads to the encounter of platelets with the ‘priming’ region (1 cm long). The ‘primed’ platelets flowed downstream where they were captured by the downstream capture region (100% fibrinogen coverage, 1 cm long)(left panel). Blocking the fibrinogen ‘priming’ region with an anti-fibrinogen polyclonal antibody attenuates the downstream adhesion response (right panel). (from Corum and Hlady, Biomaterials 33 (2012) 1255-1260).

Fig 3. Downstream platelet adhesion from whole blood was agonist dose-dependent. An increasing surface concentration of covalently attached fibrinogen (Fgn) in the ‘priming’ region resulted in increased adhesion to the downstream capture region (100 % fibrinogen coverage) (from Eichinger and Hlady, unpublished).

Fig 4. Platelet adhesion to covalently immobilized fbrinogen patterns at coverages of 20, 50, and 85%. The nonprinted region is blocked with covalently immobilized albumin. The top and middle rows contain fuorescent images (green) of fibrinogen patterns and DIC images of platelet adhesion and spreading, respectively. (A) The bottom row includes superimposed images, where at 20% platelets rarely spread and when they do their size is strictly limited by the size of the underlying fbrinogen pattern. (B) At 50%, platelets are able to spread, but their morphology almost strictly depends on the shape of the underlying fibrinogen pattern. (C) At 85%, platelets are able to spread over inert albumin regions, and the morphology is not necessarily dependent on the underlying fibrinogen pattern (from Corum, Eichinger, Hsiao and Hlady, Langmuir 2011, 27, 8316–8322).