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pubmed-article:2541141pubmed:abstractTextWhen human granulocytes that have been primed with recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSFrh) are activated by ligands that stimulate the respiratory burst, the amount of superoxide anion (O2-) they generate is significantly increased. We have found that the accelerated rate of O2- release occurring under these conditions is accompanied by an antecedent increase in membrane depolarization. We examined the nature of the enhancement of membrane depolarization in GM-CSFrh-primed granulocytes and investigated its relationship to the increase in O2- generation by N-formyl methionylleucylphenylalanine (fMLP)-activated granulocytes. We found that augmented depolarization could not be accounted for by a change in the resting membrane potential induced by the growth factor and was still present after either blocking passive transmembrane Na+ movement with dimethylamiloride or by increasing the membrane's permeability to K+ with valinomycin. When their ability to depolarize was virtually eliminated by dissipating the transmembrane K+ gradient, GM-CSFrh-pretreated cells continued to generate more O2- after fMLP than did control cells. These results indicate that augmentation of the granulocyte's ability to generate O2- anions, which is induced by priming with GM-CSFrh, is independent both of the resting transmembrane potential and of alterations in the extent of membrane potential change induced by stimuli such as fMLP.lld:pubmed
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pubmed-article:2541141pubmed:authorpubmed-author:SimonsE RERlld:pubmed
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pubmed-article:2541141pubmed:pagination361-9lld:pubmed
pubmed-article:2541141pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:2541141pubmed:articleTitleEffects of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSFrh) on transmembrane electrical potentials in granulocytes: relationship between enhancement of ligand-mediated depolarization and augmentation of superoxide anion (O2-) production.lld:pubmed
pubmed-article:2541141pubmed:affiliationDepartment of Medicine, Boston University Medical School, Massachusetts.lld:pubmed
pubmed-article:2541141pubmed:publicationTypeJournal Articlelld:pubmed
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pubmed-article:2541141pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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