A1 Refereed original research article in a scientific journal
Uptake of (11)C-Choline in Mouse Atherosclerotic Plaques
Authors: Laitinen IEK, Luoto P, Nagren K, Marjamaki PM, Silvola JMU, Hellberg S, Laine VJO, Yla-Herttuala S, Knuuti J, Roivainen A
Publisher: SOC NUCLEAR MEDICINE INC
Publication year: 2010
Journal: Journal of Nuclear Medicine
Journal name in source: JOURNAL OF NUCLEAR MEDICINE
Journal acronym: J NUCL MED
Number in series: 5
Volume: 51
Issue: 5
First page : 798
Last page: 802
Number of pages: 5
ISSN: 0161-5505
DOI: https://doi.org/10.2967/jnumed.109.071704
Abstract
The purpose of this study was to explore the feasibility of (11)C-choline in the assessment of the degree of inflammation in atherosclerotic plaques. Methods: Uptake of (11)C-choline-choline was studied ex vivo in tissue samples and aortic sections excised from 6 atherosclerotic mice deficient for both low-density lipoprotein receptor and apolipoprotein B48 (LDLR(-/-)ApoB(100/100)) and 5 control mice. The autoradiographs were compared with the immunohistology of the arterial sites. Results: The uptake of (11)C-choline-choline (percentage of the injected activity per gram of tissue) in the atherosclerotic aortas of the LDLR(-/-)ApoB(100/100) mice was significantly higher (1.9-fold, P = 0.0016) than that in the aortas of the control mice. The autoradiography analysis showed significantly higher uptake of (11)C-choline in the plaques than in healthy vessel wall (mean ratio, 2.3 +/- 0.6; P = 0.014), prominently in inflamed plaques, compared with noninflamed plaque areas. Conclusion: We observed a high (11)C-choline uptake in the aortic plaques of atherosclerotic mice. Our data suggest that macrophages may be responsible for the uptake of (11)C-choline in the plaques.
The purpose of this study was to explore the feasibility of (11)C-choline in the assessment of the degree of inflammation in atherosclerotic plaques. Methods: Uptake of (11)C-choline-choline was studied ex vivo in tissue samples and aortic sections excised from 6 atherosclerotic mice deficient for both low-density lipoprotein receptor and apolipoprotein B48 (LDLR(-/-)ApoB(100/100)) and 5 control mice. The autoradiographs were compared with the immunohistology of the arterial sites. Results: The uptake of (11)C-choline-choline (percentage of the injected activity per gram of tissue) in the atherosclerotic aortas of the LDLR(-/-)ApoB(100/100) mice was significantly higher (1.9-fold, P = 0.0016) than that in the aortas of the control mice. The autoradiography analysis showed significantly higher uptake of (11)C-choline in the plaques than in healthy vessel wall (mean ratio, 2.3 +/- 0.6; P = 0.014), prominently in inflamed plaques, compared with noninflamed plaque areas. Conclusion: We observed a high (11)C-choline uptake in the aortic plaques of atherosclerotic mice. Our data suggest that macrophages may be responsible for the uptake of (11)C-choline in the plaques.
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