Abstract: Objective To investigate the potential roles of miR-146a in effecting on platelet immune activation. Methods Using flow cytometry to detect PAC-1 and CD62-P expression level of whole blood and q-PCR and light transmittance aggre-gometry to test miR-146a expression level and platelet aggregation rate of plasma in Coronary Artery Disease (CAD) patients (n = 31) compared with controls (n = 35). In addition, an in vitro megakaryocytic maturation and platelet formation model, as measured by CD41 and CD61 through flow cytometry, has been established by using K562 cells treated with PMA induction. The mimics, inhibitor, mimics NC and inhibitor NC of miR-146a were used to study the biological function of it. Results In CAD patients the miR-146a, PAC-1 and CD62-P positive expression rate and platelet aggregation rate were increased (P<0.05) compared with controls. In addition, miR-146a leaded to enhance TLR-4, PAC-1 and CD62-P expression level (P<0.05) when challenged with miR-146a mimics. Conclusion This study has demonstrated that miR-146a can affects the platelet immune activation via TLR-s signal pathway, which imply that miR-146a might be able to act as novel tools for regulation of platelet activation.

Key words: miR-146a, TLR-4, platelet, immune activation