title: Increased plasma levels of the soluble form of Fas ligand in patients with acute myocardial infarction and unstable angina pectoris.
abstract: OBJECTIVE
  To examine whether the Fas/Fas ligand system is involved in the pathogenesis of acute myocardial infarction (AMI), we measured the levels of the soluble form of the Fas ligand (sFasL) in the plasma of patients with AMI and stable or unstable angina pectoris (AP).
  
  
  BACKGROUND
  The Fas ligand (FasL) is rapidly cleaved off by a metalloproteinase from the cell membrane to become a soluble form as a cytokine. Fas is expressed in most cells, including cardiomyocytes, whereas FasL is mainly expressed in inflammatory cells such as macrophages, which are greatly accumulated in unstable plaque.
  
  
  METHODS
  Thirty patients with AMI, 10 patients with unstable AP, 10 patients with stable AP and 30 control subjects were enrolled in the present study.
  
  
  RESULTS
  Plasma sFasL levels were significantly elevated on hospital admission in patients with AMI and unstable AP, compared with control subjects. Time-course studies revealed that plasma sFasL levels rapidly decreased within 3 h and then increased again after percutaneous transluminal coronary angioplasty in patients with AMI, but not in patients with stable AP. Importantly, the sFasL levels were higher in the coronary sinus than in the circulation. In addition, in vitro studies showed that the expression of FasL messenger ribonucleic acid was upregulated in mononuclear cells isolated from patients with AMI and that hypoxia stimulated the release of sFasL from isolated mononuclear cells.
  
  
  CONCLUSIONS
  This demonstration of elevated levels of sFasL in patients with AMI and unstable AP suggests that activation of the Fas/FasL system may play a pathogenic role in AMI and acute coronary syndromes.
authors.affiliation: Department of Geriatric Medicine, Osaka University Medical School, Suita, Japan.
authors.forename: Masumi
authors.initials: M
authors.lastname: Shimizu
authors.forename: Keisuke
authors.initials: K
authors.lastname: Fukuo
authors.forename: Shigekazu
authors.initials: S
authors.lastname: Nagata
authors.forename: Toshimitsu
authors.initials: T
authors.lastname: Suhara
authors.forename: Masashi
authors.initials: M
authors.lastname: Okuro
authors.forename: Kenshi
authors.initials: K
authors.lastname: Fujii
authors.forename: Yorihiko
authors.initials: Y
authors.lastname: Higashino
authors.forename: Masaki
authors.initials: M
authors.lastname: Mogi
authors.forename: Yasuko
authors.initials: Y
authors.lastname: Hatanaka
authors.forename: Toshio
authors.initials: T
authors.lastname: Ogihara
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood* / Q000000981:diagnostic imaging / Q000503:physiopathology*; D000789:Angina, Unstable / Q000097:blood* / Q000000981:diagnostic imaging / Q000503:physiopathology*; D017023:Coronary Angiography; D053222:Fas Ligand Protein; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000000981:diagnostic imaging / Q000503:physiopathology*; D012720:Severity of Illness Index; D012995:Solubility; D013997:Time Factors
chemical_list: C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins