Journal of Thrombosis and Thrombolysis

, Volume 33, Issue 4, pp 362–370 | Cite as

Expression of ADAMTS-2, -3, -13, and -14 in culprit coronary lesions in patients with acute myocardial infarction or stable angina

  • Cheol Whan Lee
  • Ilseon Hwang
  • Chan-Sik Park
  • Hyangsin Lee
  • Duk-Woo Park
  • Su-Jin Kang
  • Seung-Whan Lee
  • Young-Hak Kim
  • Seong-Wook Park
  • Seung-Jung ParkEmail author


ADAMTS (a disintegrin and metalloproteinase with thrombospondin type 1 motifs) proteases are emerging as key participants in the pathogenesis of vascular diseases. We studied the expression of ADAMTS-2, -3, -4 and -14 in the culprit plaques from patients presenting with acute myocardial infarction (AMI) versus stable angina. Tissue samples were gathered from 52 patients with AMI (n = 35) or stable angina (n = 17) who underwent directional coronary atherectomy. The specimens were stained with hematoxylin-eosin and analyzed immunohistochemically using antibodies specific to ADAMTS-2, -3, -13 and -14, and markers for endothelial cells, macrophages, and smooth muscle cells. Baseline characteristics of the groups were mostly similar. The proportion of smooth muscle α-actin-immunopositive area was smaller in the AMI group than in the stable angina group, but the areas immunopositive for CD31 or CD68 were higher in the AMI group. The relative areas immunopositive for ADAMTS-2, -3, and -13 in AMI were significantly larger than those in stable angina. However, the proportion of areas immunopositive for ADAMTS-14 did not differ between the two groups. Areas that stained for ADAMTS-2, -3, -13, and -14 largely overlapped with those positive for CD31 or CD68. The areas immunopositive for ADAMTS proteases were significantly correlated with CD31- or CD68-immunostained areas. In conclusions, ADAMTS-2, -3, and -13 expression, but not that of ADAMTS-14, are increased in plaques causing AMI compared those associated with stable angina. These results support a role for these enzymes in the pathogenesis of AMI.


ADAMTS protease Coronary disease Plaque stability 



This study was supported by a grant from the Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea (A090264).

Conflict of interest



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Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  • Cheol Whan Lee
    • 1
  • Ilseon Hwang
    • 2
  • Chan-Sik Park
    • 3
  • Hyangsin Lee
    • 4
  • Duk-Woo Park
    • 1
  • Su-Jin Kang
    • 1
  • Seung-Whan Lee
    • 1
  • Young-Hak Kim
    • 1
  • Seong-Wook Park
    • 1
  • Seung-Jung Park
    • 1
    • 5
    Email author
  1. 1.Department of MedicineUniversity of UlsanSeoulKorea
  2. 2.Department of Pathology, School of MedicineKeimyung UniversityDaeguKorea
  3. 3.Department of Pathology, Asan Medical CenterUniversity of UlsanSeoulKorea
  4. 4.Asan Institute of Life ScienceUniversity of UlsanSeoulKorea
  5. 5.Division of Cardiology, Asan Medical CenterUniversity of UlsanSongpa-gu, SeoulKorea

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