Targeted imaging of hypoxia-induced integrin activation in myocardium early after infarction

J Appl Physiol (1985). 2008 May;104(5):1504-12. doi: 10.1152/japplphysiol.00861.2007. Epub 2008 Mar 20.

Abstract

The alphavbeta3-integrin is expressed in angiogenic vessels in response to hypoxia and represents a potential novel target for imaging myocardial angiogenesis. This study evaluated the feasibility of noninvasively tracking hypoxia-induced alphavbeta3-integrin activation within the myocardium as a marker of angiogenesis early after myocardial infarction. Acute myocardial infarction was produced by coronary artery occlusion in rodent and canine studies. A novel (111)In-labeled radiotracer targeted at the alphavbeta3-integrin ((111)In-RP748) was used to localize regions of hypoxia-induced angiogenesis early after infarction. In rodent studies, the specificity of (111)In-RP748 for alphavbeta3-integrin was confirmed with a negative control compound ((111)In-RP790), and regional uptake of these compounds correlated with (201)Tl perfusion and a (99m)Tc-labeled nitroimidazole (BRU59-21), which was used as a quantitative marker of myocardial hypoxia. The ex vivo analysis demonstrated that only (111)In-RP748 was selectively retained in infarcted regions with reduced (201)Tl perfusion and correlated with uptake of BRU59-21. In canine studies, myocardial uptake of (111)In-RP748 was assessed using in vivo single-photon-emission computed tomography (SPECT), ex vivo planar imaging, and gamma well counting of myocardial tissue and correlated with (99m)Tc-labeled 2-methoxy-2-methyl-propyl-isonitrile ((99m)Tc-sestamibi) perfusion. Dual-radiotracer in vivo SPECT imaging of (111)In-RP748 and (99m)Tc-sestamibi provided visualization of (111)In-RP748 uptake within the infarct region, which was confirmed by ex vivo planar imaging of excised myocardial slices. Myocardial (111)In-RP748 retention was associated with histological evidence of alphavbeta3-integrin expression/activation in the infarct region. (111)In-RP748 imaging provides a novel noninvasive approach for evaluation of hypoxia-induced alphavbeta3-integrin activation in myocardium early after infarction and may prove useful for directing and evaluating angiogenic therapies in patients with ischemic heart disease.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / biosynthesis
  • Actins / genetics
  • Animals
  • Biomarkers
  • Biotransformation / physiology
  • Dogs
  • Heterocyclic Compounds, 1-Ring
  • Hypoxia / metabolism*
  • Imidazoles
  • Immunohistochemistry
  • Integrin alphaVbeta3 / biosynthesis
  • Integrin alphaVbeta3 / genetics
  • Integrins / metabolism*
  • Male
  • Myocardial Infarction / metabolism*
  • Myocardial Infarction / pathology
  • Myocardial Ischemia / pathology
  • Myocardium / metabolism*
  • Myocardium / pathology
  • Neovascularization, Physiologic / physiology
  • Organometallic Compounds
  • Organotechnetium Compounds
  • Radiopharmaceuticals
  • Rats
  • Rats, Sprague-Dawley
  • Technetium Tc 99m Sestamibi
  • Tomography, Emission-Computed, Single-Photon

Substances

  • Actins
  • BRU 59-21
  • Biomarkers
  • Heterocyclic Compounds, 1-Ring
  • Imidazoles
  • Integrin alphaVbeta3
  • Integrins
  • Organometallic Compounds
  • Organotechnetium Compounds
  • RP 748
  • Radiopharmaceuticals
  • Technetium Tc 99m Sestamibi