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*
Center For Blood Research and Department of Pathology, Harvard Medical School, Boston, MA 02115; and
Institut für Prophylaxe der Kreislaufkrankheiten, Klinikum Innenstadt, Ludwig-Maximilians-Universität, Munich, Germany
The transient regulation of very late antigen (VLA)-4 avidity by CC
chemokines may promote chemotaxis of monocytes across VCAM-1-bearing
barriers, whereas late and prolonged activation of VLA-5 may mediate
subsequent localization in the extracellular matrix. We demonstrate
that interactions of VLA-4 with VCAM-1, fibronectin, or a 40-kDa
fragment but not a 120-kDa fragment of fibronectin supported the
lateral random migration of isolated blood monocytes induced by CC
chemokines, termed chemokinesis. This effect was optimal at
intermediate substrate concentrations. Moreover, coimmobilization of
VCAM-1 with ICAM-1 allowed better migration than ICAM-1 alone.
Chemokinesis on VCAM-1 appeared to be associated with transient
regulation of VLA-4 avidity by CC chemokines, given that locking VLA-4
in a high avidity state markedly inhibited migration and the locomotion
rate was inversely correlated with the adhesive strength of VLA-4 to
VCAM-1 following stimulation with monocyte chemoattractant protein-1.
Induction of VCAM-1 expression by endothelial activation with IL-4
improved chemokinesis and lateral migration toward a monocyte
chemoattractant protein-1 or a monocyte inflammatory protein-1
gradient on endothelium and increased transendothelial chemotaxis of
monocytes by a VLA-4-dependent mechanism. In contrast, endothelial
activation with IL-4 did not affect the time required for diapedesis of
monocytes itself. Hence, VCAM-1 may facilitate transendothelial
chemotaxis by supporting lateral migration of attached monocytes along
endothelium.
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