title: Inhibition of superoxide anion production by extracellular acidification in neutrophils.
abstract: Extracellular acidification inhibited formyl-Met-Leu-Phe- or C5a-induced superoxide anion (O(2)(-)) production in differentiated HL-60 neutrophil-like cells and human neutrophils. A cAMP-increasing agonist, prostaglandin E(1), also inhibited the formyl peptide-induced O(2)(-) production. The inhibitory action on the O(2)(-) production by extracellular acidic pH was associated with cAMP accumulation and partly attenuated by H89, a protein kinase A inhibitor. A significant amount of mRNAs for T-cell death-associated gene 8 (TDAG8) and other proton-sensing ovarian cancer G-protein-coupled receptor 1 (OGR1)-family receptors is expressed in these cells. These results suggest that cAMP/protein kinase A, possibly through proton-sensing G-protein-coupled receptors, may be involved in extracellular acidic pH-induced inhibition of O(2)(-) production.
authors.affiliation: Laboratory of Signal Transduction, Institute for Molecular and Cellular Regulation Gunma University, Showa-machi, Maebashi, Japan.
authors.forename: Naoya
authors.initials: N
authors.lastname: Murata
authors.forename: Chihiro
authors.initials: C
authors.lastname: Mogi
authors.forename: Masayuki
authors.initials: M
authors.lastname: Tobo
authors.forename: Takashi
authors.initials: T
authors.lastname: Nakakura
authors.forename: Koichi
authors.initials: K
authors.lastname: Sato
authors.forename: Hideaki
authors.initials: H
authors.lastname: Tomura
authors.forename: Fumikazu
authors.initials: F
authors.lastname: Okajima
mesh_terms: D000527:Alprostadil / Q000494:pharmacology; D018797:Cell Cycle Proteins / Q000378:metabolism; D015936:Complement C5a / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism*; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism*; D005343:Fibrinolytic Agents / Q000494:pharmacology; D018922:HL-60 Cells; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007155:Immunologic Factors / Q000494:pharmacology; D007546:Isoquinolines / Q000494:pharmacology; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism*; D013449:Sulfonamides / Q000494:pharmacology; D013481:Superoxides / Q000037:antagonists & inhibitors* / Q000378:metabolism
chemical_list: D018797:Cell Cycle Proteins; D005343:Fibrinolytic Agents; C115270:G2A receptor; C091670:GPR4 protein, human; C513334:GPR65 protein, human; C486281:GPR68 protein, human; D007155:Immunologic Factors; D007546:Isoquinolines; D047428:Protein Kinase Inhibitors; D043562:Receptors, G-Protein-Coupled; D013449:Sulfonamides; D013481:Superoxides; D009240:N-Formylmethionine Leucyl-Phenylalanine; D015936:Complement C5a; D000242:Cyclic AMP; D017868:Cyclic AMP-Dependent Protein Kinases; D000527:Alprostadil; C063509:N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide