Transmembrane signaling: an ion-flux-independent model for signal transduction by complexed Fc receptors - PubMed
Transmembrane signaling: an ion-flux-independent model for signal transduction by complexed Fc receptors
L C Pfefferkorn. J Cell Biol. 1984 Dec.
Abstract
Fluxes of Na+/K+ that precede effector functions in stimulated phagocytes are thought to play a role in signal transduction. To examine this hypothesis, phagocytosis, phagosomal acidification, and superoxide anion generation (O2-) were stimulated in media in which the Na+ was replaced with K+ or choline+. Counts of particles internalized and assessment of acidification of the phagosomes by acridine orange staining indicated that Na+/K+ fluxes were not necessary for phagocytosis or phagosomal acidification in J774.2 macrophages. Phagocytosis mediated by the ionophoretic Fc receptor gamma 2b/gamma 1 of J774.2 macrophages was equally independent of a Na+ gradient. Na+/K+ fluxes did not dictate the rate of O2- generation in human monocytes. Therefore, in at least these three effector functions, Na+/K+ fluxes stimulated by Fc- and non-specific receptor binding play neither a signaling nor an enhancing role. An ion-flux-independent model for transmembrane signaling by the Fc receptor is proposed. Others have shown that there is an apparent dependence on the external Na+ concentration for O2- generation and lysosomal secretion by neutrophils. These neutrophils had been pre-treated with NH4+ during a routine purification step. O2- generation stimulated by opsonized zymosan or phorbol myristate acetate, by monocytes or monocyte-derived macrophages, and phagocytosis of opsonized zymosan by J774.2 macrophages, showed dependence on external Na+ only if these cells had been pre-treated with NH4+. Brief NH4+ pre-treatment would be expected to acidify the cytoplasm of the cells. The reversal of this acidification is known to require Na+ for H+ extrusion through the Na+/H+ antiport, thus explaining the apparent Na+ dependence.
Similar articles
-
Howell AL, Groveman DS, Wallace PK, Fanger MW. Howell AL, et al. Int J Clin Lab Res. 1997;27(2):111-7. doi: 10.1007/BF02912444. Int J Clin Lab Res. 1997. PMID: 9266281
-
Superoxide generation by human monocytes and macrophages.
Weiss SJ, King GW, LoBuglio AF. Weiss SJ, et al. Am J Hematol. 1978;4(1):1-8. doi: 10.1002/ajh.2830040102. Am J Hematol. 1978. PMID: 207181
-
Signal transduction mechanisms through Fc gamma receptors on the mouse macrophage surface.
Suzuki T. Suzuki T. FASEB J. 1991 Feb;5(2):187-93. doi: 10.1096/fasebj.5.2.1706281. FASEB J. 1991. PMID: 1706281 Review.
-
Lysosomal enzymes of phagocytes and the mechanism of their release.
Ferencík M, Stefanovic J. Ferencík M, et al. Folia Microbiol (Praha). 1979;24(6):503-15. doi: 10.1007/BF02927184. Folia Microbiol (Praha). 1979. PMID: 229064 Review. No abstract available.
Cited by
-
Intracellular pH modulates the generation of superoxide radicals by human neutrophils.
Simchowitz L. Simchowitz L. J Clin Invest. 1985 Sep;76(3):1079-89. doi: 10.1172/JCI112061. J Clin Invest. 1985. PMID: 2995444 Free PMC article.