title: Regulation of EMMPRIN (CD147) on monocyte subsets in patients with symptomatic coronary artery disease.
abstract: BACKGROUND
  The role of individual monocyte subsets in inflammatory cardiovascular diseases is insufficiently understood. Although the Extracellular Matrix Metalloproteinase Inducer (EMMPRIN) regulates important processes for inflammation such as MMP-release, its expression and regulation on monocyte subsets has not been characterized.
  
  
  METHODS
  In this clinical study, blood was obtained from 80 patients with stable coronary artery disease (CAD), 49 with acute myocardial infarction (AMI) and 34 healthy controls. Monocytes were divided into 3 subsets: CD14(++)CD16(-) (low), CD14(++)CD16(+) (intermediate), CD14(+)CD16(++) (high) according to phenotypic markers analyzed by flow cytometry. Surface expression of EMMPRIN was evaluated and compared with CD36 and CD47 expression.
  
  
  RESULTS
  In all patients, EMMPRIN expression was significantly different among monocyte subsets with the highest expression on "classical" CD14(++)CD16(-) monocytes. EMMPRIN was upregulated on all monocyte subsets in patients with AMI as compared to patients with stable CAD. Notably, neither CD47 nor CD36 revealed a significant difference in patients with AMI compared to patients with stable CAD.
  
  
  CONCLUSIONS
  EMMPRIN could serve as a marker for classical monocytes, which is upregulated in patients with acute myocardial infarction.
authors.affiliation: Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Germany.
authors.forename: Henrik
authors.initials: H
authors.lastname: Sturhan
authors.affiliation: Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Germany.
authors.forename: Saskia N I v
authors.initials: SN
authors.lastname: Ungern-Sternberg
authors.affiliation: Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Germany.
authors.forename: Harald
authors.initials: H
authors.lastname: Langer
authors.affiliation: Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Germany.
authors.forename: Meinrad
authors.initials: M
authors.lastname: Gawaz
authors.affiliation: Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Germany.
authors.forename: Tobias
authors.initials: T
authors.lastname: Geisler
authors.affiliation: Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Germany.
authors.forename: Andreas E
authors.initials: AE
authors.lastname: May
authors.affiliation: Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Germany. Electronic address: peter.seizer@med.uni-tuebingen.de.
authors.forename: Peter
authors.initials: P
authors.lastname: Seizer
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D051926:Basigin / Q000096:biosynthesis*; D018955:CD36 Antigens / Q000096:biosynthesis; D002469:Cell Separation; D003324:Coronary Artery Disease / Q000097:blood*; D005260:Female; D005434:Flow Cytometry; D058851:GPI-Linked Proteins / Q000096:biosynthesis; D005786:Gene Expression Regulation; D064368:Healthy Volunteers; D006801:Humans; D007249:Inflammation; D018950:Lipopolysaccharide Receptors / Q000096:biosynthesis; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism*; D009203:Myocardial Infarction / Q000097:blood*; D010641:Phenotype; D017452:Receptors, IgG / Q000096:biosynthesis
chemical_list: C497886:BSG protein, human; D018955:CD36 Antigens; C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D018950:Lipopolysaccharide Receptors; D017452:Receptors, IgG; D051926:Basigin
keywords: Acute coronary syndrome; CD147; Monocyte subsets