A leukocyte-mimetic magnetic resonance imaging contrast agent homes rapidly to activated endothelium and tracks with atherosclerotic lesion macrophage content

Arterioscler Thromb Vasc Biol. 2012 Jun;32(6):1427-35. doi: 10.1161/ATVBAHA.111.241844. Epub 2012 Apr 12.

Abstract

Objective: Endothelial cell activation is an important mediator of monocyte recruitment to sites of vascular inflammation. We hypothesized that high-affinity dual-ligand microparticles of iron oxide (MPIO), targeted to P-selectin and vascular cell adhesion molecule-1 (PV-MPIO), would identify activated endothelial cells during atherosclerosis progression.

Methods and results: In vivo magnetic resonance imaging in apolipoprotein E-deficient mice showed rapid binding of PV-MPIO to the aortic root, which was maximal 30 minutes post-MPIO injection and maintained at 60 minutes. Minimal binding was observed for control IgG-MPIO. Intensely low magnetic resonance signal areas, corresponding to PV-MPIO binding, were detected early (14 weeks), during foam cell formation. Contrast effects increased at 20 weeks during fibrofatty lesion development (P<0.05), but reduced by 30 weeks (P<0.01). Across all lesion severities, magnetic resonance imaging contrast effects correlated with lesion macrophage area quantified by immunohistochemistry (R=0.53; P<0.01). Near-infrared fluorescently labeled PV-MPIO were shown, by flow cytometry, to bind only activated endothelial cells and not to macrophages. Using en face immunofluorescence, we further demonstrate selective PV-MPIO accumulation at atherosclerosis-susceptible sites, with minimal binding to atherosclerosis-spared regions.

Conclusions: This high-affinity leukocyte-mimetic magnetic resonance imaging agent reveals endothelial activation. PV-MPIO demonstrate exceptionally rapid in vivo steady state accumulation, providing conspicuous magnetic resonance contrast effects that can be objectively quantified. In atherosclerosis progression, PV-MPIO tracked closely with the burden and distribution of plaque macrophages, not merely plaque size. On a biocompatible platform, this approach has potential for quantitative magnetic resonance imaging of inflammatory disease activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies
  • Antibody Affinity
  • Aorta / immunology
  • Aorta / metabolism
  • Aorta / pathology*
  • Aortic Diseases / diagnosis*
  • Aortic Diseases / genetics
  • Aortic Diseases / immunology
  • Aortic Diseases / metabolism
  • Aortic Diseases / pathology
  • Apolipoproteins E / deficiency
  • Apolipoproteins E / genetics
  • Atherosclerosis / diagnosis*
  • Atherosclerosis / genetics
  • Atherosclerosis / immunology
  • Atherosclerosis / metabolism
  • Atherosclerosis / pathology
  • Binding Sites, Antibody
  • Biomimetic Materials*
  • Contrast Media* / pharmacokinetics
  • Disease Models, Animal
  • Disease Progression
  • Endothelium, Vascular / immunology
  • Endothelium, Vascular / metabolism
  • Endothelium, Vascular / pathology*
  • Female
  • Ferric Compounds
  • Flow Cytometry
  • Humans
  • Immunohistochemistry
  • Leukocytes / immunology
  • Leukocytes / metabolism
  • Leukocytes / pathology*
  • Ligands
  • Macrophages / immunology
  • Macrophages / metabolism
  • Macrophages / pathology*
  • Magnetic Resonance Imaging*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • P-Selectin / immunology
  • P-Selectin / metabolism
  • Particle Size
  • Spectroscopy, Near-Infrared
  • Time Factors
  • Vascular Cell Adhesion Molecule-1 / immunology
  • Vascular Cell Adhesion Molecule-1 / metabolism

Substances

  • Antibodies
  • Apolipoproteins E
  • Contrast Media
  • Ferric Compounds
  • Ligands
  • P-Selectin
  • SELP protein, human
  • Vascular Cell Adhesion Molecule-1
  • ferric oxide