Platelet factor 4 , function

The technologies described above can be used to pinpoint the mechanism(s) of action of angiogenic or angiostatic agents in specific steps in the angiogenic cascade. For instance, application of these systems revealed that IFNa and angiostatin inhibit cell migration whereas endostatin and platelet factor-4 function primarily as inhibitors of endothelial cell proliferation. 

Lasagni L, Francalanci M, Annunziato F, et al. An alternatively spliced variant of CXCR3 mediates the inhibition of endothelial cell growth induced by IP-10, Mig, and I-TAC, and acts as functional receptor for platelet factor 4. J Exp Med 2003 197(11) 1537—1549. 

Eisman R, Surrey S, Ramachandran B, Schwartz E, Poncz M. Structural and functional comparison of the genes for human platelet factor 4 and PF4alt. Blood 1990 76(2) 336-344. 

Micromedex, lepirudin directly inhibits all actions of thrombin. It inhibits free and clot-bound thrombin without requiring endogenous cofactors. Lepirudin is not inhibited by platelet factor 4 and acts independently of antithrombin III and heparin cofactor II. It has no direct effect on platelet function, except inhibition of thrombin-induced platelet activation. No physiological inhibitor of lepirudin is known. 

Coagulation disorders result from a decreased number of platelets, decreased function of platelets, coagulation factor deficiency, or enhanced fibrinolytic activity. A series of complex actions and reactions of procoagulant and anticoagulant events regulate blood flow. Maintenance of blood flow involves the interplay of four major components (1) the vessel wall, (2) platelets, (3) the coagulation system, and (4) the fibrinolytic system. 

K. H. (2005) Platelet factor 4 and interleukin-8 CXC chemokine heterodimer formation modulates function at the quaternary structural level. The Journal of Biological Chemistry, 280 (6), 4948-4958. 

Several of the new chemokines—MPIF-1, MPIF-2, LARC, and SLC—have been shown to be not only chemoattractants for leukocytes, but also inhibitors of hematopoietic progenitor-cell proli-feration. These dual functions put them in a class with several other established chemokines, including MIP-la (68), MCP-1, platelet factor (PF)-4, IL-8, and GRO-P (67). 

The hemorrhagic diathesis observed in patients with uremia probably results from a defect in platelet function because of platelets inability to provide throm-boplastic substance or platelet factor IV. 

A distinct impression is emerging from the literature that nutrition plays an important role in haemostasis and thrombosis. Although present knowledge is sketchy and newer information is still needed to place nutritional-thrombotic interrelationships on a firm foundation, recent literature shows that dietary fats alter platelet function and that this might occur as a consequence of alterations of platelet lipids. Thus far, feeding studies in man and animals have shown alterations in platelet factor 3 (PF-3), platelet aggregation, and platelet lipids. 

Thrombin, the two-chain derivative of the prothrombin molecule, has a molecular weight of approximately 37,000 daltons. Its proteolytic properties induce the conversion of fibrinogen to fibrin to produce the initial visible manifestation of coagulation, the soluble fibrin clot. In addition, thrombin influences the activity of Factors V, VIII, and XIII and plasmin. Thrombin affects platelet function by inducing viscous metamorphosis and the release reaction with subsequent aggregation. 

Figure 10.11. Effectiveness factor >) as a function of Thiele modulus 4> (4> = A./, for platelet, 4> = Xrc for...

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