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Titolo:
Modulation of luminol chemiluminescence of fMet-Leu-Phe-stimulated neutrophils by affecting dephosphorylation and the metabolism of phosphatidic acid
Autore:
Arnhold, J; Benard, S; Kilian, U; Reichl, S; Schiller, J; Arnold, K;
Indirizzi:
Univ Leipzig, Fak Med, Inst Med Phys & Biophys, D-04103 Leipzig, Germany Univ Leipzig Leipzig Germany D-04103 & Biophys, D-04103 Leipzig, Germany
Titolo Testata:
LUMINESCENCE
fascicolo: 3, volume: 14, anno: 1999,
pagine: 129 - 137
SICI:
1522-7235(199905/06)14:3<129:MOLCOF>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; NADPH-OXIDASE; PHOSPHOLIPASE-D; OKADAIC ACID; HYPOCHLOROUS ACID; 2ND MESSENGERS; SUPEROXIDE RELEASE; RESPIRATORY BURST; FREE-RADICALS; CALYCULIN-A;
Keywords:
polymorphonuclear leukocytes; NADPH-oxidase; luminol; chemiluminescence; protein phosphatase inhibitors; protein kinases; phosphatidic acid;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Arnhold, J Univ Leipzig, Fak Med, Inst Med Phys & Biophys, Liebigstr 27, D-04103 Leipzig, Germany Univ Leipzig Liebigstr 27 Leipzig Germany D-04103 zig, Germany
Citazione:
J. Arnhold et al., "Modulation of luminol chemiluminescence of fMet-Leu-Phe-stimulated neutrophils by affecting dephosphorylation and the metabolism of phosphatidic acid", LUMINESCENC, 14(3), 1999, pp. 129-137

Abstract

This paper is addressed to study how PKC-mediated effects and phosphatidicacid interact together in activation of NADPH-oxidase in formyl-methionyl-leucyl-phenylalanine (fMet-Leu-Phe) stimulated neutrophils as detected by luminol chemiluminescence. The early luminescence response in fMet-Leu-Phe-stimulated cells (up to 5 min after stimulation) depends mainly on reactive oxygen species generated extracellularly, whereas all later events are caused by oxidation of luminol inside the cells. The two protein phosphatase inhibitors, okadaic acid and calyculin A, dramatically increased the late luminescence of cells. This enhancement was totally inhibited by the phospholipase D modulator butanol, while the protein kinase C (PKC) inhibitor bisindolylmaleimide I was insensitive. The early luminescence response of the cells was slightly inhibited by both protein phosphatase inhibitors and depended on protein kinase C as well as on phospholipase D activities. Propranolol, an inhibitor of phosphatidate phosphohydrolase, enhanced all parts of luminescence response of fMet-Leu-Phe-stimulated neutrophils at concentrations up to 2.5 x 10(-5) mol/L. While the late luminescence response of propranolol-treated cells was not inhibited by the PKC inhibitor bisindolylmaleimide I, the first response depended on protein kinase C. The inhibitor of diacylglycerol kinase R59949 enhanced the luminescence signal only during the first 4 min in fMet-Leu-Phe-stimulated cells. Only diacylglycerols derived from phospholipase C, such as 1-stearoyl-2-arachidonoyl-sn-glycerol, were able to initiate an oxidative burst in cells. Saturated diacylglycerols (e.g. 1,2-dipalmitoyl-sn-glycerol or 1,2-distearoyl-sn-glycerol) did not yield any luminol chemiluminescence, although they were incorporated into the plasma membrane, as evidenced by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry. Our results demonstrate that phosphatidic acid produced by phospholipase D is responsible for NADPH-oxidase activity in flMet-Leu-Phe-stimulated neutrophils over the entire measuring time, whereas PKC-mediated processes are only involved during the first 5 min. Copyright (C) 1999 John Wiley & Sons, Ltd.

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Documento generato il 04/04/20 alle ore 12:17:57