Actin polymerization induced by chemotactic peptide and concanavalin A in rat neutrophils.

Abstract

Changes in the state of actin in rat neutrophils were studied after chemotactic peptide and concanavalin A stimulation by using the DNase I inhibition assay. Actin polymerization occurred within seconds after stimulation with F-Met-Leu-Phe and concanavalin A. Pretreatment of cells with cytochalasin D prevented chemotactic peptide-induced actin polymerization. The addition of F-Met-Leu-Phe to lysed cells did not produce any change in actin state. These data offer strong evidence for receptor-induced actin polymerization and support the models implicating actin microfilament formation as a crucial event in cell activation. The observations on platelets, lymphocytes, neutrophils, and islets of Langerhans from different species suggest that actin polymerization might be a universal intracellular event accompanying cell surface receptor perturbation in eukaryotic cells.