title: Potential anti-inflammatory role of activin A in acute coronary syndromes.
abstract: OBJECTIVE
  We sought to investigate whether activin A could be involved in the immunopathogenesis of acute coronary syndromes.
  
  
  BACKGROUND
  Inflammatory mechanisms seem to play a pathogenic role in atherosclerosis and acute coronary syndromes, but the actual mediators have not been fully identified. Activin A, a pleiotropic member of the transforming growth factor-beta cytokine family, has recently been suggested to play a role in inflammation.
  
  
  METHODS
  We examined the role of activin A and its endogenous inhibitor follistatin in patients with stable (n = 26) and unstable angina (n = 20) and healthy control subjects (n = 20) by different experimental approaches.
  
  
  RESULTS
  1) Patients with stable angina had raised activin A concentrations, as assessed by protein levels in serum and messenger ribonucleic acid levels in peripheral blood mononuclear cells (PBMCs). 2) Although several activin A-related mediators were upregulated in PBMCs from patients with stable angina compared with controls (i.e., activin A and Smad3), no changes or even downregulation (i.e., Smad2) were seen in unstable disease. 3) The activin type II receptors, representing the primary ligand-binding proteins, were downregulated in unstable compared with stable angina. 4) Percutaneous coronary intervention induced a decrease in the activin A/follistatin ratio, suggesting downregulatory effects on activin A activity. 5) Although activin A dose-dependently suppressed the release of inflammatory cytokines from PBMCs in angina patients, an opposite effect was found in healthy controls.
  
  
  CONCLUSIONS
  Our findings suggest an anti-inflammatory potential of activin A in angina patients, and such effects may be of particular relevance in unstable angina in which several of the activin parameters were downregulated.
authors.affiliation: Research Institute for Internal Medicine, Rikshospitalet University Hospital, University of Oslo, Oslo, Norway.
authors.forename: Camilla
authors.initials: C
authors.lastname: Smith
authors.forename: Arne
authors.initials: A
authors.lastname: Yndestad
authors.forename: Bente
authors.initials: B
authors.lastname: Halvorsen
authors.forename: Thor
authors.initials: T
authors.lastname: Ueland
authors.forename: Torgun
authors.initials: T
authors.lastname: Waehre
authors.forename: Kari
authors.initials: K
authors.lastname: Otterdal
authors.forename: Hanne
authors.initials: H
authors.lastname: Scholz
authors.forename: Knut
authors.initials: K
authors.lastname: Endresen
authors.forename: Lars
authors.initials: L
authors.lastname: Gullestad
authors.forename: Stig S
authors.initials: SS
authors.lastname: Frøland
authors.forename: Jan Kristian
authors.initials: JK
authors.lastname: Damås
authors.forename: Påål
authors.initials: P
authors.lastname: Aukrust
mesh_terms: D028341:Activins / Q000097:blood* / Q000235:genetics / Q000502:physiology; D000789:Angina, Unstable / Q000097:blood* / Q000503:physiopathology / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000097:blood; D005260:Female; D038681:Follistatin / Q000097:blood / Q000235:genetics; D015870:Gene Expression; D006801:Humans; D007249:Inflammation; D018836:Inflammation Mediators / Q000097:blood; D028322:Inhibin-beta Subunits / Q000097:blood* / Q000235:genetics / Q000502:physiology; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000097:blood; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction; D051785:Smad Proteins; D015534:Trans-Activators / Q000097:blood
chemical_list: D016207:Cytokines; D004268:DNA-Binding Proteins; D038681:Follistatin; D018836:Inflammation Mediators; D012333:RNA, Messenger; D051785:Smad Proteins; D015534:Trans-Activators; C422405:activin A; D028341:Activins; D028322:Inhibin-beta Subunits