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The phenotype induced by ADP-ribosylation of Rho in T lymphocytes appeared different than that induced in fibroblast models, where microinjection of C3 results in fibroblast retraction of pseudopodia, with the cell body rounding up eventually to become non-adherent [ 17 ] . Video time-lapse microscopy demonstrated the elongation of aberrant pseudopods in HPB-ALL cells plated on the β1 substrate VCAM-1, rather than an altered retraction of already formed pseudopods.
It has also been reported that inhibition of endothelial nitric oxide synthases (using the non-selective NOS inhibitor L-NAME), induces endothelial adhesion molecules (ICAM-1 and VCAM-1) in HUVEC [ 24, 25].
Two immunoglobulins which are particularly important in the cell adhesion cascade are Intercellular Adhesion Molecule-1 (ICAM-1) or CD54 and Vascular Cell Adhesion Molecule-1 (VCAM-1).
When HPB-ALL cells are plated onto β1 integrin substrate such as fibronectin, vascular cell adhesion molecule-1 (VCAM-1), or even antibodies to α4β1 integrins, they respond by extending pseudopodia and displaying a highly flattened, spread morphology (figure 3, panels 4, 7, and 10, and ref [ 32 ] ). However, electroporation of C3 appeared to alter HPB-ALL morphology resulting in the extension of very fine branched finger-like cellular processes when cells were plated on the β1 integrin substrates Fn (figure 3, panel 6), VCAM-1 (figure 3, panel 9), or a mAb specific for β1 integrins (figure 3, panel 12).
The TK-1 lymphocyte cell line used in this assay expresses high levels of the alpha 4 beta 7 integrin, which can interact with multiple ligands including mucosal addressin-1 (MAdCAM-1), as well as VCAM-1, L-selectin and fibronectin [ 5].