Rao K M, Varani J
J Immunol. 1982 Oct;129(4):1605-7.
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.
通过DNase I抑制试验研究趋化肽和伴刀豆球蛋白A刺激后大鼠中性粒细胞中肌动蛋白状态的变化。用F-Met-Leu-Phe和伴刀豆球蛋白A刺激后,肌动蛋白在数秒内发生聚合。用细胞松弛素D预处理细胞可阻止趋化肽诱导的肌动蛋白聚合。向裂解细胞中添加F-Met-Leu-Phe不会使肌动蛋白状态发生任何变化。这些数据为受体诱导的肌动蛋白聚合提供了有力证据,并支持了将肌动蛋白微丝形成视为细胞激活关键事件的模型。对来自不同物种的血小板、淋巴细胞、中性粒细胞和胰岛的观察表明,肌动蛋白聚合可能是真核细胞中伴随细胞表面受体扰动的普遍细胞内事件。