title: Expression of stanniocalcin-1 in culprit coronary plaques of patients with acute myocardial infarction or stable angina.
abstract: BACKGROUND
  Stanniocalcin-1 (STC1) is involved in fundamental biological processes such as angiogenesis, inflammation and wound healing, but little is known about its expression in human coronary atherosclerotic plaques or its relationship to plaque instability.
  
  
  OBJECTIVE
  STC1 expression was examined in the culprit coronary plaques of 70 patients with acute myocardial infarction (AMI; n=49) or stable angina (n=21) who underwent directional coronary atherectomy.
  
  
  METHODS
  The specimens were stained with H&E, STC1-specific antibodies, and endothelial cells, macrophages and smooth muscle cell markers.
  
  
  RESULTS
  The baseline characteristics of the two groups of patients were largely similar. CD31-immunopositive and CD68-immunopositive areas, indicative of the presence of endothelial cells and macrophages, respectively, were proportionately larger while areas immunopositive for α-actin, as a smooth muscle cell marker, were proportionately smaller in the AMI group than in the stable angina group. The proportion of STC1-immunopositive areas was significantly greater in the AMI group than in the stable angina group (20.0% (8.2-29.0%) vs 8.8% (3.9-19.4%), p=0.022). Areas positive for STC1 were independently correlated with those immunopositive for CD31 (r=0.42, p<0.001) and CD68 (r=0.40, p<0.001). STC1 immunoreactivity co-localised with CD31-immunopositive and CD68-immunopositive cells.
  
  
  CONCLUSIONS
  STC1 is differentially expressed in the culprit coronary plaques of patients with AMI versus those with stable angina. STC1 may play a role in plaque instability.
authors.affiliation: Department of Medicine, Division of Cardiology, Heart Institute, Asan Medical Center, University of Ulsan, Seoul, Korea.
authors.forename: Cheol Whan
authors.initials: CW
authors.lastname: Lee
authors.forename: Ilseon
authors.initials: I
authors.lastname: Hwang
authors.forename: Chan-Sik
authors.initials: CS
authors.lastname: Park
authors.forename: Hyangsin
authors.initials: H
authors.lastname: Lee
authors.forename: Duk-Woo
authors.initials: DW
authors.lastname: Park
authors.forename: Soo-Jin
authors.initials: SJ
authors.lastname: Kang
authors.forename: Seung-Whan
authors.initials: SW
authors.lastname: Lee
authors.forename: Young-Hak
authors.initials: YH
authors.lastname: Kim
authors.forename: Seong-Wook
authors.initials: SW
authors.lastname: Park
authors.forename: Seung-Jung
authors.initials: SJ
authors.lastname: Park
mesh_terms: D000328:Adult; D000368:Aged; D060050:Angina, Stable / Q000378:metabolism* / Q000473:pathology; D003331:Coronary Vessels / Q000378:metabolism* / Q000473:pathology; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology; D005260:Female; D006023:Glycoproteins / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D008264:Macrophages / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000378:metabolism* / Q000473:pathology; D058226:Plaque, Atherosclerotic / Q000378:metabolism* / Q000473:pathology
chemical_list: D006023:Glycoproteins; C051795:teleocalcin