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00925njm 22002777a 4500 dc Tahara, Nobuhiro author Zandbergen, H. Reinier author de Haas, Hans J. author Petrov, Artiom author Pandurangi, Raghu author Yamaki, Takayoshi author Zhou, Jun author Imaizumi, Tsutomu author Slart, Riemer H. J. A. author Dyszlewski, Mary author Scarabelli, Tiziano author Kini, Annapoorna author Reutelingsperger, Chris author Narula, Navneet author Fuster, Valentin author Narula, Jagat author 2014 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. In-111-GSAO uptake was observed within the regions of apoptosis seeking agent-(99)mTc-Annexin A5 uptake, suggesting the colocalization of apoptotic and necrotic cell death processes. Sci Rep. 2014; 4:6826 2045-2322 http://hdl.handle.net/20.500.12105/5538 25351258 10.1038/srep06826 Scientific Reports INCREASED CARDIOMYOCYTE APOPTOSIS SHOCK PROTEIN-90 ALKYLATOR REPERFUSION INJURY HEART-FAILURE ANNEXIN A5 DILATED CARDIOMYOPATHY ISCHEMIC-MYOCARDIUM MAGNETIC-RESONANCE IN-VIVO MECHANISMS Noninvasive Molecular Imaging of Cell Death in Myocardial Infarction using In-111-GSAO