2026-04-29T04:08:51Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/55382024-10-31T11:58:44Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
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
funder
Banyu Life Science Foundation International
funder
Dutch Heart Association
funder
National Institutes of Health (Estados Unidos)
2017-12-01T07:37:29Z
2017-12-01T07:37:29Z
2014
Sci Rep. 2014; 4:6826
2045-2322
http://hdl.handle.net/20.500.12105/5538
25351258
10.1038/srep06826
Scientific Reports
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.
eng
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
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NoninvasiveMolecularImagingofCell_2014_suppl.docx
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NoninvasiveMolecularImagingofCell_2014.pdf.txt
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