Endothelial cells are important cells in inflammatory responses (1, 2). Bacterial lipopolysaccharides (LPS), viruses, inflammation, and tissue injury increase secretion of tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), and other cytokines and chemokines. Emigration of leukocytes from blood is dependent on their ability to roll along endothelial cell surfaces and subsequently adhere to endothelial cell surfaces. Inflammatory mediators and cytokines induce chemokine secretion from endothelial cells and other vascular cells and increase their expression of cell-surface adhesion molecules, such as intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), integrins, and selectins. Chemokines are chemotactic toward leukocytes and sites of inflammation and tissue injury. The movements of leukocytes through endothelial junctions into the extravascular space are highly orchestrated through various interactions with different adhesion molecules on endothelial cells (3).
VCAM-1 is found in very low levels (often non-detectable) on the cell surface of resting endothelial cells and other vascular cells, such as smooth muscle cells and fibroblasts (4-8). VCAM-1 binds to its counterligand integrin, very late antigen-4 (VLA-4), on the cell surface of leukocytes. Inflammatory cytokines, such as IL-1 and TNF-α, increase expression of VCAM-1 and other cell adhesion molecules on the vascular endothelial cells, which leads to leukocyte adhesion to the activated endothelium. Furthermore, VCAM-1 expression was also induced by oxidized low-density lipoproteins under atherogenic conditions (1). Overexpression of VCAM-1 by atherosclerotic lesions plays an important role in their progression toward vulnerable plaques, which may erode and rupture. A synthetic peptide (Arg-Glu-Asn-Leu-Arg-Ile-Ala-Leu-Arg-Tyr, B2702-p) corresponding to residues 75–84 of HLA-B2702 was shown to bind specifically to VCAM-1 (9). 123I-Labelingof B2702-p was performed on the tyrosine (residue 84) using the chloramine-T method (10). 123I-labeled B2702-p is being developed as a non-invasive agent for VCAM-1 expression in vascular endothelial cells during different stages of inflammation in atherosclerosis.