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Differential expression of oxidation-specific epitopes and apolipoprotein(a) in progressing and ruptured human coronary and carotid atherosclerotic lesions

Academic Article
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Overview

authors

  • van Dijk, R. A.
  • Kolodgie, F.
  • Ravandi, A.
  • Leibundgut, G.
  • Hu, P. P.
  • Prasad, A.
  • Mahmud, E.
  • Dennis, E.
  • Curtiss, Linda
  • Witztum, J. L.
  • Wasserman, B. A.
  • Otsuka, F.
  • Virmani, R.
  • Tsimikas, S.

publication date

  • December 2012

journal

  • Journal of Lipid Research  Journal

abstract

  • The relationships between oxidation-specific epitopes (OSE) and lipoprotein (a) [Lp(a)] and progressive atherosclerosis and plaque rupture have not been determined. Coronary artery sections from sudden death victims and carotid endarterectomy specimens were immunostained for apoB-100, oxidized phospholipids (OxPL), apo(a), malondialdehyde-lysine (MDA), and MDA-related epitopes detected by antibody IK17 and macrophage markers. The presence of OxPL captured in carotid and saphenous vein graft distal protection devices was determined with LC-MS/MS. In coronary arteries, OSE and apo(a) were absent in normal coronary arteries and minimally present in early lesions. As lesions progressed, apoB and MDA epitopes did not increase, whereas macrophage, apo(a), OxPL, and IK17 epitopes increased proportionally, but they differed according to plaque type and plaque components. Apo(a) epitopes were present throughout early and late lesions, especially in macrophages and the necrotic core. IK17 and OxPL epitopes were strongest in late lesions in macrophage-rich areas, lipid pools, and the necrotic core, and they were most specifically associated with unstable and ruptured plaques. Specific OxPL were present in distal protection devices. Human atherosclerotic lesions manifest a differential expression of OSEs and apo(a) as they progress, rupture, and become clinically symptomatic. These findings provide a rationale for targeting OSE for biotheranostic applications in humans.

subject areas

  • Apolipoproteins A
  • Atherosclerosis
  • Biomarkers
  • Carotid Artery Diseases
  • Epitopes
  • Female
  • Humans
  • Male
  • Middle Aged
  • Oxidation-Reduction
  • Plaque, Atherosclerotic
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Identity

PubMed Central ID

  • PMC3494262

International Standard Serial Number (ISSN)

  • 0022-2275

Digital Object Identifier (DOI)

  • 10.1194/jlr.P030890

PubMed ID

  • 22969153
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Additional Document Info

start page

  • 2773

end page

  • 2790

volume

  • 53

issue

  • 12

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