Receptor-stimulated actin polymerization requires cytoplasmic acidification in human PMNs.
Cytoplasmic alkalinization has received considerable attention as a regulatory event In cell growth, transformation and signal transduction (Busa, W.B. (1986) Annu. Rev. Physiol. 48, 389-402 and Moolenar, W.H. (1986) Annu. Rev. Physiol. 48, 363-376). In contrast the current paper presents evidence for the role of an early cytoplasmic acidification, during signal transduction in the polymorphonuclear leukocyte (PMN). Following PMN stimulation with a chemotactic peptide, there is a significant decrease in cytoplasmic pH concomitant with a dramatic increase in cytoskeletal actin. The data indicate that this drop in pHi is necessary, but not sufficient, for signal transduction leading to cytoskeletal reorganization in these cells.
Harvard School of Dental Medicine, Forsyth Dental Center, Boston, MA 02115.
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M
Tonetti
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M
Budnick
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Niederman
D000199:Actins / Q000378:metabolism*; D002465:Cell Movement; D003593:Cytoplasm / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007700:Kinetics; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism*; D015398:Signal Transduction
D000199:Actins; D009240:N-Formylmethionine Leucyl-Phenylalanine