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ADAMTS-7 is associated with a high-risk plaque phenotype in human atherosclerosis

Author:
  • Eva Bengtsson
  • Karin Hultman
  • Pontus Dunér
  • Giuseppe Asciutto
  • Peter Almgren
  • Marju Orho-Melander
  • Olle Melander
  • Jan Nilsson
  • Anna Hultgårdh
  • Isabel Gonçalves
Publishing year: 2017-12-01
Language: English
Publication/Series: Scientific Reports
Volume: 7
Issue: 1
Document type: Journal article
Publisher: Nature Publishing Group

Abstract english

Several large-scale genome-wide association studies have identified single-nucleotide polymorphisms in the genomic region of A Disintegrin And Metalloproteinase with ThromboSpondin type 1 repeats (ADAMTS)-7 and associations to coronary artery disease. Experimental studies have provided evidence for a functional role of ADAMTS-7 in both injury-induced vascular neointima formation and development of atherosclerotic lesions. However, whether ADAMTS-7 is associated with a specific plaque phenotype in humans has not been investigated. Carotid plaques (n = 206) from patients with and without cerebrovascular symptoms were analyzed for expression of ADAMTS-7 by immunohistochemistry and correlated to components associated with plaque vulnerability. Plaques from symptomatic patients showed increased levels of ADAMTS-7 compared with lesions from asymptomatic patients. High levels of ADAMTS-7 correlated with high levels of CD68-staining and lipid content, but with low smooth muscle cell and collagen content, which together are characteristics of a vulnerable plaque phenotype. ADAMTS-7 levels above median were associated with increased risk for postoperative cardiovascular events. Our data show that ADAMTS-7 is associated with a vulnerable plaque phenotype in human carotid lesions. These data support previous observations of a potential proatherogenic role of ADAMTS-7.

Keywords

  • Cardiac and Cardiovascular Systems

Other

Published
  • Cardiovascular Research - Immunity and Atherosclerosis
  • Genomics, Diabetes and Endocrinology
  • Diabetes - Cardiovascular Disease
  • Cardiovascular Research - Hypertension
  • Vessel Wall Biology
  • ISSN: 2045-2322
E-mail: jan [dot] nilsson [at] med [dot] lu [dot] se

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