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Noninvasive molecular imaging of cell death in myocardial infarction using 111In-GSAO
Nobuhiro Tahara1, H Reinier Zandbergen2, Hans J de Haas3
1Division of Cardio-Vascular Medicine, Department of Medicine, Kurume University School of Medicine, Kurume, Japan.
Abstract:
Acute insult to the myocardium is associated with substantial loss of cardiomyocytes during the process of myocardial infarction. In this setting, apoptosis (programmed cell death) and necrosis may operate on a continuum. Because the latter is characterized by the loss of sarcolemmal integrity, we propose that an appropriately labeled tracer directed at a ubiquitously present intracellular moiety would allow non-invasive definition of cardiomyocyte necrosis. A trivalent arsenic peptide, GSAO (4-(N-(S-glutathionylacetyl)amino)phenylarsonous acid), is capable of binding to intracellular dithiol molecules such as HSP90 and filamin-A. Since GSAO is membrane impermeable and dithiol molecules abundantly present intracellularly, we propose that myocardial localization would represent sarcolemmal disruption or necrotic cell death. In rabbit and mouse models of myocardial infarction and post-infarct heart failure, we employed In-111-labelled GSAO for noninvasive radionuclide molecular imaging. (111)In-GSAO uptake was observed within the regions of apoptosis seeking agent- (99m)Tc-Annexin A5 uptake, suggesting the colocalization of apoptotic and necrotic cell death processes.
Insights
This study introduces a novel tracer, GSAO, for non-invasively detecting cardiomyocyte necrosis after myocardial infarction. The tracer
Area of Science:
- Cardiovascular Research
- Molecular Imaging
- Biomedical Engineering
Background:
- Myocardial infarction leads to significant cardiomyocyte loss through apoptosis and necrosis.
- Distinguishing between apoptosis and necrosis is crucial for understanding heart damage.
- Current methods for assessing cardiomyocyte death are often invasive or lack specificity.
Purpose of the Study:
- To develop and validate a novel non-invasive imaging agent for detecting cardiomyocyte necrosis.
- To assess the feasibility of using a labeled trivalent arsenic peptide, GSAO, for this purpose.
- To investigate the colocalization of necrotic and apoptotic cell death in myocardial infarction models.
Main Methods:
- Development of an Indium-111 labeled trivalent arsenic peptide (GSAO).
- Administration of (111)In-GSAO in rabbit and mouse models of myocardial infarction and heart failure.
- Non-invasive radionuclide molecular imaging to assess myocardial uptake of the tracer.
- Comparison of (111)In-GSAO uptake with a known apoptosis-seeking agent, (99m)Tc-Annexin A5.
Main Results:
- Myocardial uptake of (111)In-GSAO was observed in regions consistent with myocardial injury.
- The uptake of (111)In-GSAO colocalized with regions showing uptake of (99m)Tc-Annexin A5.
- This colocalization suggests that both necrotic and apoptotic cell death processes occur concurrently.
Conclusions:
- The membrane-impermeable tracer (111)In-GSAO shows promise for non-invasively identifying cardiomyocyte necrosis.
- This molecular imaging approach can help define the extent of cell death in myocardial infarction.
- The findings support the use of GSAO as a tool to study the continuum of cell death in cardiac injury.
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