Article Text

PDF
Expression of stanniocalcin-1 in culprit coronary plaques of patients with acute myocardial infarction or stable angina
  1. Cheol Whan Lee1,
  2. Ilseon Hwang2,
  3. Chan-Sik Park3,
  4. Hyangsin Lee4,
  5. Duk-Woo Park1,
  6. Soo-Jin Kang1,
  7. Seung-Whan Lee1,
  8. Young-Hak Kim1,
  9. Seong-Wook Park1,
  10. Seung-Jung Park1
  1. 1Department of Medicine, Division of Cardiology, Heart Institute, Asan Medical Center, University of Ulsan, Seoul, Korea
  2. 2Department of Pathology, School of Medicine, Keimyung University, Choong-Ku, Daegu, Korea
  3. 3Department of Pathology, Asan Medical Center, Seoul, Korea
  4. 4Asan Institute of Life Science, University of Ulsan, Seoul, Korea
  1. Correspondence to Dr Seung-Jung Park, Division of Cardiology, Heart Institute, Asan Medical Center, University of Ulsan, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, Korea; sjpark{at}amc.seoul.kr

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.

Keywords

Statistics from Altmetric.com

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.