Surface fibrinogen

Alpha helices are sufficiently versatile to produce many very different classes of structures. In membrane-bound proteins, the regions inside the membranes are frequently a helices whose surfaces are covered by hydrophobic side chains suitable for the hydrophobic environment inside the membranes. Membrane-bound proteins are described in Chapter 12. Alpha helices are also frequently used to produce structural and motile proteins with various different properties and functions. These can be typical fibrous proteins such as keratin, which is present in skin, hair, and feathers, or parts of the cellular machinery such as fibrinogen or the muscle proteins myosin and dystrophin. These a-helical proteins will be discussed in Chapter 14. 

Platelets are the formed elements of the blood which participate in hemostasis. Platelets are enucleated, discoid fragments which arise from mature megakaryocytes in the bone marrow. Under normal circumstances, platelets do not adhere to endothelial surfaces of blood vessels. However, platelets can adhere to damaged areas of blood vessels and become activated in such a way that they can also bind fibrinogen. 

Chen et al. utUized a direct chemical reaction with a given solution (wet treatment) to modify the surface of the silicone rubber. The presence of a layer of PEO on a biomaterial surface is accompanied by reductions in protein adsorption, and cell and bacterial adhesion. In order to obtain a PEO layer on top of the silicone rabber surface, the surface was firstly modihed by incorporating an Si-H bond using (MeHSiO) , and followed by PEO grafting to the surface using a platinum-catalyzed hydrosilylation reaction. These PEO-modified surfaces were demonstrated by fibrinogen adsorption both from buffer and plasma, as well as albumin adsorption from buffer. Reductions in protein adsorption of as much as 90% were noted on these surfaces. 

In a similar study, adriamycin was incorporated into fibrinogen microspheres. In contrast to 5-FU, adriamycin released slowly from the matrix for up to 7 days, with little evidence of burst. This difference is probably attributable to the lack of surface release of adriamycin as evidenced by the unchanged nature of the microsphere surface. 

HK it can interact with surface-bound factor XII on an adjacent particle thereby disseminating the reaction [25, 28]. As a result the effective kallikrein/factor XII ratio is increased in the presence of HK [25], Finally, in plasma, HK can displace other adhesive glycoproteins such as fibrinogen from binding to the surface [29]. In this sense, HK, like factor XII and prekallikrein, is also a coagulation cofactor because it is required for the generation of kalUkrein (a factor XII activator) as well as the activation of factor XI. 

Schmaier AH. Silver L. Adams AL, Fischer GC, Munoz PC, Vroman L, et al The effect of high molecular weight kininogen on surface-adsorbed fibrinogen. Thromb Res 1984 33 51-67. 

Initiation of the fibrin clot in response to tissue injury is carried out by the extrinsic pathway. How the intrinsic pathway is activated in vivo is unclear, but it involves a negatively charged surface. The intrinsic and extrinsic pathways converge in a final common path-vray involving the activation of prothrombin to thrombin and the thrombin-catalyzed cleavage of fibrinogen to form the fibrin clot. The intrinsic, extrinsic, and final common pathways are complex and involve many different proteins (Figure 51-1 and Table 51-1). In... 

SM O Connor, SH Gehrke, S Patuto, GS Retzinger. Fibrinogen-dependent adherence of macrophages to surfaces coated with poly(ethylene oxide)/poly(propylene oxide) triblock copolymers. Ann NY Acad Sci 831 138-144, 1997. 

Tegoulia VA, Rao W, Kalambur AT, Rabolt JF, Cooper SL (2001) Surface properties, fibrinogen adsorption, and cellular interactions of a novel phosphorylcholine-containing self-assembled monolayer on gold. Langmuir 17 4396-4404... 

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