2006

DOI: 10.1161/01.atv.0000200106.34016.18

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¹⁸ F-Choline Images Murine Atherosclerotic Plaques Ex Vivo

Christian M. Matter

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,

Matthias T. Wyss

²

,

Patricia Stutzmann Meier

³

et al.

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Alternative Strategies For Imaging Vascular Inflammation1

Harvest and Tissue Processing1

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Cited by 104 publications

(72 citation statements)

References 30 publications

(51 reference statements)

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“…We observed high uptake in the heart and kidneys, which could be problematic when imaging these targets. However, there seems to be a species difference, because low myocardial uptake has been previously reported in humans (7,9). Choline and its metabolites such as betaine or acetylcholine may have a different cardiac uptake pattern in rodents.…”

Section: Discussionmentioning

confidence: 94%

Uptake of ¹¹C-Choline in Mouse Atherosclerotic Plaques

et al. 2010

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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 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 2/2 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 (percentage of the injected activity per gram of tissue) in the atherosclerotic aortas of the LDLR 2/2 ApoB 100/100 mice was significantly higher (1.9-fold, P 5 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 6 0.6; P 5 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.

“…We observed high uptake in the heart and kidneys, which could be problematic when imaging these targets. However, there seems to be a species difference, because low myocardial uptake has been previously reported in humans (7,9). Choline and its metabolites such as betaine or acetylcholine may have a different cardiac uptake pattern in rodents.…”

Section: Discussionmentioning

confidence: 94%

Uptake of ¹¹C-Choline in Mouse Atherosclerotic Plaques

et al. 2010

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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 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 2/2 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 (percentage of the injected activity per gram of tissue) in the atherosclerotic aortas of the LDLR 2/2 ApoB 100/100 mice was significantly higher (1.9-fold, P 5 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 6 0.6; P 5 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.

“…Recently, studies have suggested that the quality rather than quantity of macrophages is critical in the evolution of vulnerable plaques (27)(28)(29). M1 macrophages play a key role in the development of atherosclerosis, which is mediated by production of proinflammatory cytokines or reactive nitrogen oxides, whereas M2 macrophages have antiatherogenic properties mediated by the production of antiinflammatory cytokines and the suppression of proinflammatory signaling (30,31).…”

Section: Discussionmentioning

confidence: 99%

Comparison of Contrast Agents for Atherosclerosis Imaging Using Cultured Macrophages: FDG Versus Ultrasmall Superparamagnetic Iron Oxide

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et al. 2013

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Various noninvasive imaging methods have been developed to evaluate atherosclerotic plaques. Among them, 18 F-FDG PET and MR imaging with ultrasmall superparamagnetic iron oxide particles (USPIO) have been used to quantify plaque inflammation. Both methods are based on the efficient uptake of FDG and USPIO by macrophages in atherosclerotic lesions. Differently polarized macrophages have been reported to have different characteristics that are involved in the pathologic development of atherosclerosis. M1 polarized macrophages are considered the more proatherogenic phenotype than M2 polarized macrophages. However, little is known regarding the association between macrophage polarization and FDG or USPIO accumulation. In this study, we investigated intracellular FDG and USPIO accumulation in M1 and M2 polarized macrophages. Methods: THP-1 macrophages were differentiated into M1 and M2 polarized macrophages. Under optimal glucose conditions, we investigated the 3 H-labeled FDG uptake in M1 and M2 polarized macrophages. We then investigated intracellular USPIO uptake by M1 and M2 macrophages. Results: We found that M1 polarization, compared with M2 polarization, results in increased intracellular accumulation of FDG. To elucidate the mechanism by which FDG was preferentially accumulated in M1 macrophages, we examined messenger RNA expressions of glucose transporters (GLUTs) and hexokinases, which have pivotal roles in glucose uptake, and glucose-6-phosphatase (G6Pase), which catalyzes the reverse reaction of hexokinase. In M1 macrophages, GLUT-1, GLUT-3, hexokinase 1, and hexokinase 2 were upregulated and G6Pase was downregulated. In contrast to FDG, M1 polarization resulted in decreased intracellular accumulation of USPIO. We found that scavenger receptor A and CD11b, which are involved in USPIO binding and uptake, were significantly downregulated by M1 polarization. Conclusion: Compared with M2, proatherogenic M1 macrophages preferentially accumulated FDG but not USPIO, suggesting that FDG PET is a useful method for the detection of proinflammatory M1 macrophages.

“…Labelled choline was not taken up into normal vascular wall, or purely calcified lesions, in a retrospective analysis of 93 male patients undergoing cancer imaging [101]. In ex vivo imaging of aortae of ApoE-deficient mice, [ 18 F]-fluorocholine uptake better correlated with fat staining and macrophage-positive areas than FDG [102]. Computed tomography imaging of molecular targets is hampered by a significantly lower sensitivity than PET, but provides much better spatial and temporal resolution.…”

Section: Alternative Strategies For Imaging Vascular Inflammationmentioning

confidence: 99%

Vascular imaging with positron emission tomography

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²

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et al. 2011

Journal of Internal Medicine

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Atherosclerosis is an inflammatory disease that causes most myocardial infarctions, strokes and acute coronary syndromes. Despite the identification of multiple risk factors and widespread use of drug therapies, it still remains a global health concern with associated costs. Although angiography is established as the gold standard means of detecting coronary artery stenosis, it does not image the vessel wall itself, reporting only on its consequences such as luminal narrowing and obstruction. MRI and computed tomography provide more information about the plaque structure, but recently positron emission tomography (PET) imaging using [ 18 F]-fluorodeoxyglucose (FDG) has been advocated as a means of measuring arterial inflammation. This results from the ability of FDG-PET to highlight areas of high glucose metabolism, a feature of macrophages within atherosclerosis, particularly in high-risk plaques. It is suggested that the degree of FDG accumulation in the vessel wall reflects underlying inflammation levels and that tracking any changes in FDG uptake over time or with drug therapy might be a way of getting an early efficacy readout for novel anti-atherosclerotic drugs. Early reports also demonstrate that FDG uptake is correlated with the number of cardiovascular risk factors and possibly even the risk of future cardiovascular events. This review will outline the evidence base, shortcomings and emerging applications for FDG-PET in vascular imaging. Alternative PET tracers and other candidate imaging modalities for measuring vascular inflammation will also be discussed.

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