Chronic myeloid leukemia granulocytes exhibit reduced actin polymerization after chemotactic peptide stimulation.

Abstract

Polymorphonuclear leukocytes (PMNL) from chronic myeloid leukemia (CML) patients are defective for chemotaxis in response to the synthetic chemotactic peptide n-formyl-methionyl-leucyl-phenylalanine (fMLP) as compared to normal PMNL. The present study investigated whether the defective chemotactic response was mediated through altered actin polymerization induced with fMLP. Granulocytes isolated from seven normal subjects and seven CML patients were stimulated with fMLP and lysed with Triton containing buffer at time points of 0, 30 seconds, and 1, 2, and 10 minutes. The Triton insoluble cytoskeleton containing polymerized actin was analyzed by SDS-PAGE and densitometry. The CML PMNL polymerized significantly lesser actin than normal PMNL on stimulation with 10 nM (p > 0.05) and 1 nM (p > 0.01) fMLP. This lower actin polymerization observed in fMLP-stimulated CML PMNL may be responsible for the defective chemotaxis seen in these cells.