| Literature DB >> 24412923 |
Nobuhiro Tahara1, Jogeshwar Mukherjee2, Hans J de Haas3, Artiom D Petrov4, Ahmed Tawakol5, Nezam Haider4, Atsuko Tahara6, Cristian C Constantinescu, Jun Zhou, Hendrikus H Boersma7, Tsutomu Imaizumi6, Masataka Nakano8, Aloke Finn9, Zahi Fayad4, Renu Virmani8, Valentin Fuster10, Lisardo Bosca11, Jagat Narula4.
Abstract
Progressive inflammation in atherosclerotic plaques is associated with increasing risk of plaque rupture. Molecular imaging of activated macrophages with 2-deoxy-2-[(18)F]fluoro-D-glucose ([(18)F]FDG) has been proposed for identification of patients at higher risk for acute vascular events. Because mannose is an isomer of glucose that is taken up by macrophages through glucose transporters and because mannose receptors are expressed on a subset of the macrophage population in high-risk plaques, we applied (18)F-labeled mannose (2-deoxy-2-[(18)F]fluoro-D-mannose, [(18)F]FDM) for targeting of plaque inflammation. Here, we describe comparable uptake of [(18)F]FDM and [(18)F]FDG in atherosclerotic lesions in a rabbit model; [(18)F]FDM uptake was proportional to the plaque macrophage population. Our FDM competition studies in cultured cells with 2-deoxy-2-[(14)C]carbon-D-glucose ([(14)C]2DG) support at least 35% higher [(18)F]FDM uptake by macrophages in cell experiments. We also demonstrate that FDM restricts binding of anti-mannose receptor antibody to macrophages by approximately 35% and that mannose receptor targeting may provide an additional avenue for imaging of plaque inflammation.Entities:
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Year: 2014 PMID： 24412923 DOI： 10.1038/nm.3437
Source DB: PubMed Journal: Nat Med ISSN： 1078-8956 Impact factor: 53.440