title: Comparison of ADAMTS-1, -4 and -5 expression in culprit plaques between acute myocardial infarction and stable angina.
abstract: BACKGROUND
  ADAMTS (a disintegrin and metalloproteinase with thrombospondin type 1 motifs) proteases might contribute to plaque destabilisation by weakening the fibrous cap. However, little is known about the expression of ADAMTS proteases in coronary atherosclerotic plaques.
  
  
  OBJECTIVE
  To examine the expression of ADAMTS proteases in coronary atherectomy samples obtained from patients with acute myocardial infarction (AMI) or stable angina.
  
  
  METHODS
  Atherectomy specimens were obtained from 34 patients with AMI (n=23) or stable angina (n=11) who underwent directional coronary atherectomy. The specimens were stained with H&E and analysed immunohistochemically using antibodies specific to ADAMTS-1, -4 and -5; versican cleavage products; and markers for endothelial cells, macrophages and smooth muscle cells.
  
  
  RESULTS
  Baseline characteristics were similar between the two groups. The proportion of CD31 and CD68 immunopositive areas did not differ between the two groups, but the area immunopositive for smooth muscle α-actin was smaller in the AMI group. The relative area immunopositive for ADAMTS-1 in AMI (1.04% (IQR 0.59-2.09%)) was significantly greater than that in stable angina (0.24% (0.15-0.39%); p<0.001). In contrast, the proportion of areas immunopositive for ADAMTS-4 or -5 was similar in the two groups. Areas that stained for ADAMTS-1 largely overlapped with those positive for CD68 and versican cleavage products. The areas immunopositive for ADAMTS-1 were significantly correlated with CD68 immunostained areas (r=0.50, p=0.003).
  
  
  CONCLUSIONS
  ADAMTS-1, -4 and -5 were present in human coronary atherosclerotic plaques, and ADATS-1 was more strongly expressed in AMI plaques than in stable plaques. ADAMTS-1 may play a role in plaque instability.
authors.affiliation: Department of Medicine, 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: Su-Jin
authors.initials: SJ
authors.lastname: Kang
authors.forename: Seung-Hwan
authors.initials: SH
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: D051722:ADAM Proteins / Q000378:metabolism*; D000071097:ADAMTS1 Protein; D000071121:ADAMTS4 Protein; D000071116:ADAMTS5 Protein; D000208:Acute Disease; D000328:Adult; D000368:Aged; D000787:Angina Pectoris / Q000150:complications / Q000378:metabolism*; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D017225:Atherectomy, Coronary; D003331:Coronary Vessels / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000378:metabolism*; D058226:Plaque, Atherosclerotic / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D011348:Procollagen N-Endopeptidase / Q000378:metabolism; D000097382:CD68 Molecule
chemical_list: D051722:ADAM Proteins; D000071097:ADAMTS1 Protein; D000071121:ADAMTS4 Protein; D000071116:ADAMTS5 Protein; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D011348:Procollagen N-Endopeptidase; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C103859:ADAMTS1 protein, human; C121532:ADAMTS5 protein, human; C000603918:ADAMTS4 protein, human