VCAM-1 Target in Non-Invasive Imaging for the Detection of Atherosclerotic Plaques

Abstract

Atherosclerosis is a progressive chronic arterial disease characterised by atheromatous plaque formation in the intima of the arterial wall. Several invasive and non-invasive imaging techniques have been developed to detect and characterise atherosclerosis in the vessel wall: anatomic/structural imaging, functional imaging and molecular imaging. In molecular imaging, vascular cell adhesion molecule-1 (VCAM-1) is a promising target for the non-invasive detection of atherosclerosis and for the assessment of novel antiatherogenic treatments. VCAM-1 is an adhesion molecule expressed on the activated endothelial surface that binds leucocyte ligands and therefore promotes leucocyte adhesion and transendothelial migration. Hence, for several years, there has been an increase in molecular imaging methods for detecting VCAM-1 in MRI, PET, SPECT, optical imaging and ultrasound. The use of microparticles of iron oxide (MPIO), ultrasmall superparamagnetic iron oxide (USPIO), microbubbles, echogenic immunoliposomes, peptides, nanobodies and other nanoparticles has been described. However, these approaches have been tested in animal models, and the remaining challenge is bench-to-bedside development and clinical applicability.

Nanobody: a promising toolkit for molecular imaging and disease therapy

“…VCAM-1 is a good target for the detection of existing atherosclerosis due to its highest abundance among atherosclerosis-related adhesion molecules. It is also useful for the detection of activated endothelium at the risk of developing plaques, because VCAM-1 is a major participant during the initiation of atherosclerosis [61,62]. Simultaneously, given that VCAM1 is involved in many other immunological disorders, the horizon of anti-VCAM1 nanobody applications can be further expanded [63].…”

Effect of Oxidized Low-Density Lipoprotein on Head and Neck Squamous Cell Carcinomas

“…Atherosclerosis is the principal cause of CVD, defined as a chronic and progressive inflammatory state due to an immune response and an uncontrolled proliferation of vascular smooth muscle cells leading to the production of pro-inflammatory cytokines [ 3 ]. Activated endothelial cells express adhesion molecules on their surface such as vascular cell adhesion molecule-1 (VCAM-1) that bind leucocyte ligands and therefore promote leucocyte adhesion and transendothelial migration [ 4 ]. This inflammatory state is mainly caused by oxidized low-density lipoproteins (oxLDLs) that activate inflammasomes to produce IL-1β in endothelial cells, monocytes/macrophages and T cells [ 3 ].…”

Sinomenine in Cardio-Cerebrovascular Diseases: Potential Therapeutic Effects and Pharmacological Evidences

“…Long-term chronic inflammation throughout atherosclerosis triggers the assembly and activation of immune cells in the lesions of atherosclerotic plaque, thus contributing to the progress of atherosclerosis (23). Inflammatory responses in vascular endothelial cells (VECs) can prompt the excretion of pro-inflammatory cytokines, activation of multiple signal pathways, and expression of endothelial leukocyte adhesion molecules including E-selectin, intracellular adhesion molecule-1 (ICAM-1), and vascular adhesion molecule-1 (VCAM-1) (14,24,25). These cellular activities are responsible for immune responses which play vital roles in the development of atherosclerosis, such as recruitment, invasion, and differentiation of monocytes, and inflammatory activities mediated by macrophages and other leukocytes (15,23).…”

“…VCAM-1, expresses and distributes on the activated VECs surface, is a kind of adhesion molecules and can bind to leukocytes and promote their adhesion and trans-endothelial migration (25,26,32). Cytokines such as tumor necrosis factor-α (TNF-α) and interleukin (IL)-1 play important roles in stimulating the expression of adhesion molecules including VCAM-1 (33).…”

“…Cytokines such as tumor necrosis factor-α (TNF-α) and interleukin (IL)-1 play important roles in stimulating the expression of adhesion molecules including VCAM-1 (33). As VCAM-1 usually indicates the infiltration of leukocytes such as monocyte, macrophage, or lymphocyte, it is thought to be a promising target to detect atherosclerosis and assess the efficacy of anti-atherogenic therapies (25). Sinomenine is found to inhibit VCAM-1 expression induced by TNF-α in VECs (26).…”