Bioactive Sphingolipids, Complement Cascade, and Free Hemoglobin Levels in Stable Coronary Artery Disease and Acute Myocardial Infarction

Background Acute myocardial infarction (AMI) and coronary artery bypass graft (CABG) surgery are associated with a pathogen-free inflammatory response (sterile inflammation). Complement cascade (CC) and bioactive sphingolipids (BS) are postulated to be involved in this process. Aim The aim of this study was to evaluate plasma levels of CC cleavage fragments (C3a, C5a, and C5b9), sphingosine (SP), sphingosine-1-phosphate (S1P), and free hemoglobin (fHb) in AMI patients treated with primary percutaneous coronary intervention (pPCI) and stable coronary artery disease (SCAD) undergoing CABG. Patients and Methods The study enrolled 37 subjects (27 male) including 22 AMI patients, 7 CABG patients, and 8 healthy individuals as the control group (CTRL). In the AMI group, blood samples were collected at 5 time points (admission to hospital, 6, 12, 24, and 48 hours post pPCI) and 4 time points in the CABG group (6, 12, 24, and 48 hours post operation). SP and S1P concentrations were measured by high-performance liquid chromatography (HPLC). Analysis of C3a, C5a, and C5b9 levels was carried out using high-sensitivity ELISA and free hemoglobin by spectrophotometry. Results The plasma levels of CC cleavage fragments (C3a and C5b9) were significantly higher, while those of SP and S1P were lower in patients undergoing CABG surgery in comparison to the AMI group. In both groups, levels of CC factors showed no significant changes within 48 hours of follow-up. Conversely, SP and S1P levels gradually decreased throughout 48 hours in the AMI group but remained stable after CABG. Moreover, the fHb concentration was significantly higher after 24 and 48 hours post pPCI compared to the corresponding postoperative time points. Additionally, the fHb concentrations increased between 12 and 48 hours after PCI in patients with AMI. Conclusions Inflammatory response after AMI and CABG differed regarding the release of sphingolipids, free hemoglobin, and complement cascade cleavage fragments.

[1]  Dirk Sieger,et al.  Complement as a regulator of adaptive immunity , 2017, Seminars in Immunopathology.

[2]  J. Camm,et al.  Cardiac effects of amiselimod compared with fingolimod and placebo: results of a randomised, parallel‐group, phase I study in healthy subjects , 2017, British journal of clinical pharmacology.

[3]  N. Frangogiannis,et al.  Immune cells in repair of the infarcted myocardium , 2017, Microcirculation.

[4]  I. Préda,et al.  Alternative complement pathway activation during invasive coronary procedures in acute myocardial infarction and stable angina pectoris. , 2016, Clinica chimica acta; international journal of clinical chemistry.

[5]  A. Subudhi,et al.  Sphingosine-1-phosphate promotes erythrocyte glycolysis and oxygen release for adaptation to high-altitude hypoxia , 2016, Nature Communications.

[6]  T. Hornemann,et al.  Decreased phosphatidylcholine plasmalogens--A putative novel lipid signature in patients with stable coronary artery disease and acute myocardial infarction. , 2016, Atherosclerosis.

[7]  T. Blom,et al.  Trafficking and Functions of Bioactive Sphingolipids: Lessons from Cells and Model Membranes , 2015, Lipid insights.

[8]  B. Dahlbäck,et al.  Quantification of sphingosine 1-phosphate by validated LC-MS/MS method revealing strong correlation with apolipoprotein M in plasma but not in serum due to platelet activation during blood coagulation , 2015, Analytical and Bioanalytical Chemistry.

[9]  P. Scarborough,et al.  Corrigendum to: cardiovascular disease in Europe 2014: epidemiological update. , 2015, European heart journal.

[10]  S. Fidan,et al.  The relationship between rheumatoid factor levels and coronary artery lesion complexity and severity in patients with stable coronary artery disease , 2015, Postepy w kardiologii interwencyjnej = Advances in interventional cardiology.

[11]  H. Langer,et al.  Platelets and the complement cascade in atherosclerosis , 2015, Front. Physiol..

[12]  M. Ratajczak A novel view of the adult bone marrow stem cell hierarchy and stem cell trafficking , 2014, Leukemia.

[13]  M. Ratajczak,et al.  Complement Component 3 is Necessary to Preserve Myocardium and Myocardial Function in Chronic Myocardial Infarction , 2014, Stem cells.

[14]  N. Frangogiannis,et al.  The inflammatory response in myocardial injury, repair, and remodelling , 2014, Nature Reviews Cardiology.

[15]  M. Ratajczak,et al.  Novel evidence that crosstalk between the complement, coagulation and fibrinolysis proteolytic cascades is involved in mobilization of hematopoietic stem/progenitor cells (HSPCs) , 2014, Leukemia.

[16]  M. Ratajczak,et al.  Novel evidence for enhanced stem cell trafficking in antipsychotic-naïve subjects during their first psychotic episode. , 2014, Journal of psychiatric research.

[17]  A. Lisowska,et al.  Dose-dependent effect of aspirin on the level of sphingolipids in human blood. , 2013, Advances in medical sciences.

[18]  L. Badimón,et al.  Coordinated proteomic signature changes in immune response and complement proteins in acute myocardial infarction: the implication of serum amyloid P-component. , 2013, International journal of cardiology.

[19]  Peter Scarborough,et al.  Cardiovascular disease in Europe 2014: epidemiological update. , 2013, European heart journal.

[20]  R. Hall Identification of inflammatory mediators and their modulation by strategies for the management of the systemic inflammatory response during cardiac surgery. , 2013, Journal of cardiothoracic and vascular anesthesia.

[21]  D. Kreisel,et al.  Processes of Sterile Inflammation , 2013, The Journal of Immunology.

[22]  M. Ratajczak,et al.  An emerging link in stem cell mobilization between activation of the complement cascade and the chemotactic gradient of sphingosine-1-phosphate. , 2013, Prostaglandins & other lipid mediators.

[23]  M. Ratajczak,et al.  Bioactive lipids and cationic antimicrobial peptides as new potential regulators for trafficking of bone marrow-derived stem cells in patients with acute myocardial infarction. , 2013, Stem cells and development.

[24]  S. Stringer,et al.  Serum sphingolipids level as a novel potential marker for early detection of human myocardial ischaemic injury , 2013, Front. Physiol..

[25]  John D Lambris,et al.  Complement in Action: An Analysis of Patent Trends from 1976 Through 2011 , 2012, Advances in experimental medicine and biology.

[26]  Peter K. Smith,et al.  Complement Activation and Cardiac Surgery: A Novel Target for Improving Outcomes , 2012, Anesthesia and analgesia.

[27]  R. Rieben,et al.  Role of complement and perspectives for intervention in ischemia-reperfusion damage , 2012, Annals of medicine.

[28]  A. Tang,et al.  Is a fully heparin-bonded cardiopulmonary bypass circuit superior to a standard cardiopulmonary bypass circuit? , 2012, Interactive cardiovascular and thoracic surgery.

[29]  Grace Y Chen,et al.  Sterile inflammation: sensing and reacting to damage , 2010, Nature Reviews Immunology.

[30]  John D Lambris,et al.  Molecular Intercommunication between the Complement and Coagulation Systems , 2010, The Journal of Immunology.

[31]  P. Bruni,et al.  An Active Form of Sphingosine Kinase-1 Is Released in the Extracellular Medium as Component of Membrane Vesicles Shed by Two Human Tumor Cell Lines , 2010, Journal of oncology.

[32]  J. G. van der Hoeven,et al.  The complement system is activated in a biphasic pattern after coronary artery bypass grafting. , 2010, The Annals of thoracic surgery.

[33]  T. Hla,et al.  Inhibitory Role of Sphingosine 1-Phosphate Receptor 2 in Macrophage Recruitment during Inflammation , 2009, The Journal of Immunology.

[34]  A. Lisowska,et al.  Plasma sphingosine-1-phosphate concentration is reduced in patients with myocardial infarction. , 2009, Medical science monitor : international medical journal of experimental and clinical research.

[35]  O. Wagner,et al.  Local complement activation triggers neutrophil recruitment to the site of thrombus formation in acute myocardial infarction , 2009, Thrombosis and Haemostasis.

[36]  S. Coughlin,et al.  Sphingosine-1-phosphate in the plasma compartment regulates basal and inflammation-induced vascular leak in mice. , 2009, The Journal of clinical investigation.

[37]  K. Dickstein,et al.  C-reactive protein, infarct size, microvascular obstruction, and left-ventricular remodelling following acute myocardial infarction. , 2009, European heart journal.

[38]  J. Brown,et al.  Sphingosine-1-phosphate receptor signalling in the heart. , 2008, Cardiovascular research.

[39]  W. Jessup Lipid metabolism: sources and stability of plasma sphingosine-1-phosphate. , 2008, Current opinion in lipidology.

[40]  G. Owens,et al.  Sphingosine-1-Phosphate Receptor Subtypes Differentially Regulate Smooth Muscle Cell Phenotype , 2008, Arteriosclerosis, thrombosis, and vascular biology.

[41]  B. Levkau Sphingosine-1-phosphate in the regulation of vascular tone: a finely tuned integration system of S1P sources, receptors, and vascular responsiveness. , 2008, Circulation research.

[42]  S. Gundewar,et al.  Sphingolipid therapy in myocardial ischemia-reperfusion injury. , 2008, Biochimica et biophysica acta.

[43]  Yusuf A. Hannun,et al.  Principles of bioactive lipid signalling: lessons from sphingolipids , 2008, Nature Reviews Molecular Cell Biology.

[44]  M. Tani,et al.  Lack of sphingosine 1-phosphate-degrading enzymes in erythrocytes. , 2007, Biochemical and biophysical research communications.

[45]  B. Levkau,et al.  The Sphingosine-1-Phosphate Analogue FTY720 Reduces Atherosclerosis in Apolipoprotein E–Deficient Mice , 2007, Arteriosclerosis, thrombosis, and vascular biology.

[46]  S. Milstien,et al.  Shooting the messenger: oxidative stress regulates sphingosine-1-phosphate. , 2007, Circulation research.

[47]  J. Chun,et al.  Sphingosine-1-Phosphate Stimulates the Functional Capacity of Progenitor Cells by Activation of the CXCR4-Dependent Signaling Pathway via the S1P3 Receptor , 2006, Arteriosclerosis, thrombosis, and vascular biology.

[48]  T. Woodruff,et al.  Complement mediators in ischemia-reperfusion injury. , 2006, Clinica chimica acta; international journal of clinical chemistry.

[49]  R. Proia,et al.  Extracellular export of sphingosine kinase-1a contributes to the vascular S1P gradient. , 2006, The Biochemical journal.

[50]  John D Lambris,et al.  Generation of C5a in the absence of C3: a new complement activation pathway , 2006, Nature Medicine.

[51]  W. Giles,et al.  Sphingosine-1-phosphate effects on guinea pig atrial myocytes: Alterations in action potentials and K+ currents. , 2006, Cardiovascular research.

[52]  P. Hess,et al.  Systemic inflammatory response to coronary artery bypass graft surgery. , 2005, American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists.

[53]  A. Parrill,et al.  S1P1-selective in vivo-active agonists from high-throughput screening: off-the-shelf chemical probes of receptor interactions, signaling, and fate. , 2005, Chemistry & biology.

[54]  Elias A. Rahal,et al.  Serum C-Reactive Protein and Complement Proteins in Patients with Acute Myocardial Infarction , 2005, Immunopharmacology and immunotoxicology.

[55]  L. Hsu Heparin-coated cardiopulmonary bypass circuits: current status , 2001, Perfusion.

[56]  D. S. Moore,et al.  The Basic Practice of Statistics , 2001 .

[57]  J. Janatova,et al.  Activation and control of complement, inflammation, and infection associated with the use of biomedical polymers. , 2000, ASAIO journal.

[58]  J. Platt,et al.  Endothelial cell activation by pore-forming structures: pivotal role for interleukin-1alpha. , 2000, Circulation.

[59]  K. Claffey,et al.  Vascular Endothelial Cell Adherens Junction Assembly and Morphogenesis Induced by Sphingosine-1-Phosphate , 1999, Cell.

[60]  P. Ward,et al.  C5a-dependent up-regulation in vivo of lung vascular P-selectin. , 1997, Journal of immunology.

[61]  J. Warren,et al.  The membrane attack complex of complement induces interleukin-8 and monocyte chemoattractant protein-1 secretion from human umbilical vein endothelial cells. , 1996, The American journal of pathology.

[62]  S. Hakomori,et al.  Sphingosine-1-phosphate: a platelet-activating sphingolipid released from agonist-stimulated human platelets. , 1995, Blood.

[63]  S. Meri,et al.  Time course of complement activation and inhibitor expression after ischemic injury of rat myocardium. , 1994, The American journal of pathology.

[64]  T. Springer,et al.  Adherence of neutrophils to cultured human microvascular endothelial cells. Stimulation by chemotactic peptides and lipid mediators and dependence upon the Mac-1, LFA-1, p150,95 glycoprotein family. , 1989, The Journal of clinical investigation.

[65]  R. Skidgel,et al.  Protamine inhibits plasma carboxypeptidase N, the inactivator of anaphylatoxins and kinins. , 1989, Anesthesiology.

[66]  D. Mathey,et al.  Deposition of the terminal C5b-9 complement complex in infarcted areas of human myocardium. , 1986, Journal of immunology.

[67]  H. Jacob,et al.  Oxygen radicals mediate endothelial cell damage by complement-stimulated granulocytes. An in vitro model of immune vascular damage. , 1978, The Journal of clinical investigation.

[68]  F. T. Hunter,et al.  A spectrophotometric method for quantitating hemoglobin in plasma or serum. , 1950, American journal of clinical pathology.

[69]  B. Dołęgowska,et al.  [Overview of methods used for determination of selected sphingolipids in different biological materials]. , 2014, Postepy biochemii.

[70]  T. Walther,et al.  Sphingosine-1-phosphate as a potential target for the treatment of myocardial infarction. , 2014, Circulation journal : official journal of the Japanese Circulation Society.

[71]  M. Kazatchkine,et al.  Activation of the complement system at the interface between blood and artificial surfaces. , 1988, Biomaterials.