Coordinated proteomic signature changes in immune response and complement proteins in acute myocardial infarction: The implication of serum amyloid P-component

Background: Patient outcomes after acute myocardial infarction (AMI) are influenced by the combined activation of several distinct interrelated signaling pathways. Specifically acute-phase response proteins can neutralize inflammatory agents, minimize the extent of tissue damage, and participate in tissue repair and regeneration. We have investigated the evolution of immune response and complement system-related proteins in the early and late phase post-AMI and their potential association with tissue damage after the ischemic event. Methods: Serum was analyzed by 2D-electrophoresis and mass-spectrometry (MALDI-TOF/TOF) in controls and de novo AMI-patients within the first 6 h after onset (admission time), and 3 days after. Results: Among differential proteins two functional groups showed coordinated changes: immune response-inflammation (alpha-1B-glycoprotein, fetuin-A, serum amyloid P-component (SAP), and complex-forming glycoprotein HC) and complement system (C1r, C3 and factor-B). Immune-related proteins showed a decrease 3 days after admission except for SAP that depicted a progressive increase from the early phase. Specifically, fetuin-A decrease was associated with the extent of myocardial necrosis. C1r and C3 were increased in the early phase with a subsequent decrease 3 days after, being C1r levels at admission correlated with necrosis and troponin-T and GPT levels. Contrarily, factor-B was decreased in the early and late phase post-AMI. Conclusions: Our results demonstrate that in the late phase post-AMI there is a coordinated decrease in immune response-inflammation proteins, except for SAP which showed an increase related to the specific activation of the classical complement pathway. Changes in immunity and complement-related proteins affect the severity of organ damage influencing prognosis after AMI. (C) 2013 Elsevier Ireland Ltd. All rights reserved.