Visualization of Vascular Inflammation in the Atherosclerotic Mouse by Ultrasmall Superparamagnetic Iron Oxide Vascular Cell Adhesion Molecule-1–Specific Nanoparticles
Marta MichalskaLina H. MachtoubHelga D. MantheyElisabeth BauerVolker HeroldGeorg KrohneGunthard LykowskyMarkus F. HildenbrandThomas KampfPeter M. JakobAlma ZerneckeWolfgang R. Bauer
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Abstract:
Noninvasive imaging of atherosclerosis remains challenging in clinical applications. Here, we applied noninvasive molecular imaging to detect vascular cell adhesion molecule-1 in early and advanced atherosclerotic lesions of apolipoprotein E-deficient mice.Ultrasmall superparamagnetic iron oxide particles functionalized with (P03011) or without (P3007) vascular cell adhesion molecule-1-binding peptide were visualized by ultra high-field (17.6 T) magnetic resonance. Injection of P03011 resulted in a marked signal loss in the aortic root of apolipoprotein E-deficient mice fed a Western diet for 8 and 26 weeks in vivo and ex vivo, compared with preinjection measurements, P3007-injected mice, and P03011- or P3007-injected age-matched C57BL/6 controls. Histological analyses revealed iron accumulations in the intima, in colocalization with vascular cell adhesion molecule-1-expressing macrophages and endothelial cells. Coherent anti-Stokes Raman scattering microscopy demonstrated iron signals in the intima and media of the aortic root in the P03011-injected but not untreated apolipoprotein E-deficient mice, localized to macrophages, luminal endothelial-like cells, and medial regions containing smooth muscle cells. Electron microscopy confirmed iron particles enclosed in endothelial cells and in the vicinity of smooth muscle cells.Using a combination of innovative imaging modalities, in this study, we demonstrate the feasibility of applying P03011 as a contrast agent for imaging of atherosclerosis.Keywords:
Ex vivo
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Intercellular adhesion molecule
Nectin
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E-selectin
VCAM-1
Cell–cell interaction
Proinflammatory cytokine
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Objective To explore the impact of mutational adenomatous polyposis coli(APC) on cell-matrix,cell-cell adhesion and the relative mechanism.Methods Cell-matrix and cell-cell adhesion assays were employed to determine the adhesion level of two stable cell lines MDCK-N2-APC and MDCK-GFP.The truncated APC of N2 fragment,which spans residues 449-781,was studied in comparison with control cells including GFP alone.Immunofluorescence staining,RT-PCR analysis and Western blot were applied to check several adhesion molecules which are key roles in cell contact process.Results In contract with control,cell-matrix adhesion was averagely increased to 180% in N2 cells,whereas cell-cell adhesion was reduced by about 30%.Our experiments accordingly indicated that CD29 expression level was enhanced and the expression level of E-cadherin was enervated in N2 cells.And these two molecules all have crucial roles in cell-matrix and cell-cell adhesion.Conclusions Full length APC plays a crucial role in cell-matrix and cell-cell adhesion.Truncated N2-APC may influence cell adhesion through changing the expression level of certain adhesion molecules,such as E-cadherin and CD29.The truncation mutation of APC fragment N2 restrained in the colon cancer cells will alter the cell invasion and migration by affecting cell adhesion and cell-matrix adhesion.
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The way in which cells communicate with each other is fundamentally important for developing and maintaining normal tissue structure and function. In order to get a better understanding of cell adhesion, researchers have long been trying to identify and characterize chemical structures at the cell surface that might participate in, or mediate, cell-cell and cell-matrix adhesion. During the last decade, this has led to the identification of a number of cell-surface adhesion proteins and their ligands, which may be either proteins or carbohydrates. The LEC cell-adhesion molecule family is a group of cell-adhesion molecules with a lectinlike domain. They bind to carbohydrate structures, some of which have been identified on dendritic cells in oral epithelium. LEC cell-adhesion molecules are found on endothelial cells during inflammation and may, in such situations, be involved in the recruiting of dendritic and other inflammatory cells, thereby playing a role in the regulation of inflammatory reactions in the oral mucosa. The integrin family is another group of cell-surface adhesion molecules recently identified in oral mucosa that participate in cell-matrix and cell-cell adhesion in many important processes including wound healing, immunodefense mechanisms, and oncogenic transformation. Knowledge of the distribution of cell-adhesion molecules and their ligands and of the mechanism that controls their expression is, therefore, of great importance in understanding of the development of disease in the oral mucosa.
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Abstract This unit provides protocols to assay cell‐cell adhesion and adhesive‐dependent cellular functions mediated by calcium‐independent adhesion molecules. These protocols have been developed for neural cell adhesion molecules of the Ig superfamily. However, most of the protocols allow a more general application to other categories of adhesion molecules and non‐neural cells.
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Adhesion plays a central role as a recognition system, guiding the interaction between individual cells, and thereby regulating many biological processes. Adhesion can occur via cell-cell or cell-extracellular matrix interactions through several major cell adhesion molecule (CAM) families, including selectins, integrins, immunoglobulins and cadherins. Recent studies have focused on the elucidation of adhesive ligands responsible for the different types of cellular adhesion. Significant breakthroughs in CAM research are a result of various developments, including the purification of various adhesive proteins from different tissue sources and cloned adhesion molecules, the generation of specific monoclonal antibodies, the development of functional assays and the identification of certain genetic disorders linked to CAM defects. This has led to an increased understanding of the importance of CAM as a key therapeutic target.
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Considerable advances have been made in our knowledge of the molecular structure of cell adhesion molecules, their binding sites, and adhesion complexes. For the cadherins, protein zero, and CD2, additional experimental data support the insights obtained from structural analysis of their domains and molecular models of their adhesion complexes. For neural cell adhesion molecules, L1, fibronectin, tenascin-C, integrins, and vascular cell adhesion molecules, the molecular structure of domains, and in most cases their binding sites, have been elucidated. The substrate recognition sites in some of these molecules possess rate constants for association and dissociation that permit both rapid cell migration and, through avidity, high-affinity cell-cell interactions.
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