Eur Heart J Cardiovasc Imaging

2016

DOI: 10.1093/ehjci/jev346

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Targeting of vascular cell adhesion molecule-1 by¹⁸F-labelled nanobodies for PET/CT imaging of inflamed atherosclerotic plaques

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Anneleen Blykers

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Catarina Xavier

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et al.

Abstract: The [(18)F]-FB-anti-VCAM-1 Nb, cross-reactive for both mouse and human VCAM-1, allows non-invasive PET/CT imaging of VCAM-1 expression in atherosclerotic plaques in a murine model and may represent an attractive tool for imaging vulnerable atherosclerotic plaques in patients.

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Ab-based Nanomaterials For Targeting Vcam In Vivo1

Tehnike Hibridnog Oslikavanja1

Vascular Cell Adhesion Molecule1

Imaging Of Inflammation At the Organ Level1

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Cited by 86 publications

(52 citation statements)

References 38 publications

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“…Bala 56 In vivo PET/CT imaging of ApoE À/À mice showed that cABCAM-1-5 were highly expressed in atherosclerotic lesions. Ex vivo analysis showed an increased uptake of targeted nanobodies in aortas 2.7 times higher than in control mice and 4.3 times higher compared to non-targeting nanobodies.…”

Section: Ab-based Nanomaterials For Targeting Vcam In Vivomentioning

confidence: 99%

Targeting cell adhesion molecules with nanoparticles using in vivo and flow-based in vitro models of atherosclerosis

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et al. 2017

Exp Biol Med (Maywood)

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Impact statementAs atherosclerosis remains the leading cause of death, there is an urgent need to develop better tools for treatment of the disease. The ability to improve current treatments relies on enhancing the accuracy of in vitro and in vivo atherosclerotic models. While in vivo models provide all the relevant testing parameters, variability between animals and among models used is a barrier to reproducible results and comparability of NP efficacy. In vitro cultures isolate cells into microenvironments that fail to take into account flow separation and shear stress, which are characteristics of atherosclerotic lesions. Flow-based in vitro models provide more physiologically relevant platforms, bridging the gap between in vivo and 2D in vitro models. This is the first review that presents recent advances regarding endothelial cell-targeting using adhesion molecules in light of in vivo and flow-based in vitro models, providing insights for future development of optimal strategies against atherosclerosis. AbstractAtherosclerosis is a leading cause of death worldwide; in addition to lipid dysfunction, chronic arterial wall inflammation is a key component of atherosclerosis. Techniques that target cell adhesion molecules, which are overexpressed during inflammation, are effective methods to detect and treat atherosclerosis. Specifically, research groups have identified vascular cell adhesion molecule-1, intercellular adhesion molecule-1, platelet endothelial cell adhesion molecule, and selectins (E-selectin and P-selectin) as correlated to atherogenesis. In this review, we discuss recent strategies both in vivo and in vitro that target cell adhesion molecules. First, we discuss peptide-based and antibody (Ab)-based nanoparticles utilized in vivo for diagnostic, therapeutic, and theranostic applications. Second, we discuss flow-based in vitro models that serve to reduce the traditional disadvantages of in vivo studies such as variability, time to develop the disease, and ethical burden, but preserve physiological relevance. The knowledge gained from these targeting studies can be translated into clinical solutions for improved detection, prevention, and treatment of atherosclerosis.

“…Bala 56 In vivo PET/CT imaging of ApoE À/À mice showed that cABCAM-1-5 were highly expressed in atherosclerotic lesions. Ex vivo analysis showed an increased uptake of targeted nanobodies in aortas 2.7 times higher than in control mice and 4.3 times higher compared to non-targeting nanobodies.…”

Section: Ab-based Nanomaterials For Targeting Vcam In Vivomentioning

confidence: 99%

Targeting cell adhesion molecules with nanoparticles using in vivo and flow-based in vitro models of atherosclerosis

¹

,

²

,

³

et al. 2017

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

Impact statementAs atherosclerosis remains the leading cause of death, there is an urgent need to develop better tools for treatment of the disease. The ability to improve current treatments relies on enhancing the accuracy of in vitro and in vivo atherosclerotic models. While in vivo models provide all the relevant testing parameters, variability between animals and among models used is a barrier to reproducible results and comparability of NP efficacy. In vitro cultures isolate cells into microenvironments that fail to take into account flow separation and shear stress, which are characteristics of atherosclerotic lesions. Flow-based in vitro models provide more physiologically relevant platforms, bridging the gap between in vivo and 2D in vitro models. This is the first review that presents recent advances regarding endothelial cell-targeting using adhesion molecules in light of in vivo and flow-based in vitro models, providing insights for future development of optimal strategies against atherosclerosis. AbstractAtherosclerosis is a leading cause of death worldwide; in addition to lipid dysfunction, chronic arterial wall inflammation is a key component of atherosclerosis. Techniques that target cell adhesion molecules, which are overexpressed during inflammation, are effective methods to detect and treat atherosclerosis. Specifically, research groups have identified vascular cell adhesion molecule-1, intercellular adhesion molecule-1, platelet endothelial cell adhesion molecule, and selectins (E-selectin and P-selectin) as correlated to atherogenesis. In this review, we discuss recent strategies both in vivo and in vitro that target cell adhesion molecules. First, we discuss peptide-based and antibody (Ab)-based nanoparticles utilized in vivo for diagnostic, therapeutic, and theranostic applications. Second, we discuss flow-based in vitro models that serve to reduce the traditional disadvantages of in vivo studies such as variability, time to develop the disease, and ethical burden, but preserve physiological relevance. The knowledge gained from these targeting studies can be translated into clinical solutions for improved detection, prevention, and treatment of atherosclerosis.

“…Bala and colleagues used PET-CT and fluorine-18 labelled vascular cell adhesion molecule (VCAM)-1 (anti-VCAM-1 nanobody, cAbVCAM-1-5), to demonstrate the feasibility in a murine-atherosclerotic model to detect aortic plaque inflammation. 45 Increased tracer uptake was detected in aortic regions with increased atherosclerosis both on PET-CT and on histology. This is just one of the many studies ongoing to obtain further insight in differences between vulnerable and stable atherosclerotic plaques.…”

Section: Tehnike Hibridnog Oslikavanjamentioning

confidence: 94%

The year in cardiology 2016: imaging

et al. 2017

Cardiologia Croatica

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“…Vascular cell adhesion molecule 1 (VCAM1) plays an important role in the initial steps of monocyte recruitment to atherosclerotic lesions, and targeted imaging of VCAM1 with 18 F-labeled anti-VCAM1 antibody has been used in preclinical studies to visualize atherosclerotic plaque (26). The high specificity of this tracer for binding with VCAM1 makes it an attractive molecular imaging agent for identification of inflamed atherosclerotic plaque.…”

Section: Vascular Cell Adhesion Moleculementioning

confidence: 99%

Molecular Imaging of Vulnerable Coronary Plaque: A Pathophysiologic Perspective

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et al. 2017

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Atherothrombotic events in coronary arteries are most often due to rupture of unstable plaque resulting in myocardial infarction. Radiolabeled molecular imaging tracers directed toward cellular targets that are unique to unstable plaque can serve as a powerful tool for identifying high-risk patients and for assessing the potential of new therapeutic approaches. Two commonly available radiopharmaceuticals-18 F-FDG and 18 F-NaF-have been used in clinical research for imaging coronary artery plaque, and ongoing clinical studies are testing whether there is an association between 18 F-NaF uptake and future atherothrombotic events. Other, less available, tracers that target macrophages, endothelial cells, and apoptotic cells have also been tested in small groups of patients. Adoption of molecular imaging of coronary plaque into clinical practice will depend on overcoming major hurdles, ultimately including evidence that the detection of unstable plaque can change patient management and improve outcomes. Cardi ovascular disease is the number one cause of death in the United States, despite numerous advances in prevention, diagnosis, and treatment (1). Nearly half these deaths are due to acute myocardial infarction, and up to 75% of myocardial infarctions are the result of an acute thrombotic event after rupture of coronary artery plaque. Rupture-prone plaques often do not cause significant obstruction (2) and are not detectable by stress imaging, the approach most commonly used to assess risk. Identification of the rupture-prone, or vulnerable, plaque could add prognostic value and thus has become a major focus in cardiovascular diagnostics. Molecular imaging with radiopharmaceuticals has the potential to play a key role in the assessment of vulnerable plaque. In this review, we will describe advances in molecular imaging in the context of the pathophysiology associated with plaque growth and vulnerability. TECHNICAL CHALLENGES IN PET IMAGING OF CORONARY PLAQUEImaging of coronary plaque with PET tracers is difficult because of the limited spatial resolution of PET, the small size of coronary plaque, and blurring caused by cardiac and respiratory motion. To partially mitigate motion of the coronary arteries, some investigators have performed enddiastolic imaging using only a part of the PET scan, but at the expense of increased image noise (3). We are exploring computational motion correction techniques that can potentially improve image quality, and we have demonstrated that these corrections can increase the target-to-background ratios of tracer uptake within coronary plaque and reduce image noise. The approach is likely to improve detection of small foci of tracer uptake within the coronary arteries (4). THE BIOLOGY OF CORONARY PLAQUEAtherosclerotic plaque develops in response to endothelial injury and entry of low-density-lipoprotein cholesterol into the intimal layer of the vessel wall. In response to this injury, monocytes are recruited into the vessel wall and differentiate into macrophages, which take up modifi...

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