The Effect of SAA-Derived Fragment — SAA_2–82 — On Platelet Aggregation

Abstract

SAA is a highly conserved acute phase protein among animals. Various inflammatory stimuli induce vigorous synthesis of SAA, which comprises up to 2.5% of the hepatic protein synthesis capacity. Despite the ubiquity of SAA and the existance of such elaborate synthetic mechanism, the biological functions of SAA remain obscure. FMF patients are subjected to recurrent inflammatory attacks, which impose physiological and biochemical changes, that are associated with propensity to cardiovascular morbidity. However, this anticipation is being challenged by the clinical observation of significantly reduced prevalence of myocardial infarctions and thromboembolic phenomena among these patients. We evaluated the potential cardioprotective effect of SAA via a tentative platelet anti-aggregatory effect. Platelet-rich plasma was pre-incubated for 20 minutes with SAA fragment, corresponding to residues 2-82, and thereafter were treated with four different aggregating agents, namely Epinephrine, Ristocetine, Collagen, and ADP. SAA-fragment, especially in its higher concentrations, was found to inhibit signficantly the normal pattern of platelet aggregation with all these four aggregants. SAA, by its platelet inhibitory property, particularly in an acute-phase response like concentration, may regulate various clinical expressions of cardiovascular morbidity. This effect should not be limited to FMF patients.