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Göteborgs universitets publikationer

Neutrophil NADPH-oxidase activation by an annexin AI peptide is transduced by the formyl peptide receptor (FPR), whereas an inhibitory signal is generated independently of the FPR family receptors

Författare och institution:
Jennie Karlsson (Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning); Huamei Fu (Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning); F. Boulay (-); Claes Dahlgren (Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning); Kristoffer Hellstrand (Institutionen för laboratoriemedicin, Avdelningen för klinisk virologi); Charlotta Movitz (Institutionen för laboratoriemedicin, Avdelningen för klinisk virologi)
Publicerad i:
Journal of leukocyte biology, 78 ( 3 ) s. 762-71
0741-5400 (Print)
Artikel, refereegranskad vetenskaplig
Sammanfattning (abstract):
Truncation of the N-terminal part of the calcium-regulated and phospholipid-binding protein annexin AI has been shown to change the functional properties of the protein and to generate immunoregulatory peptides. Proinflammatory as well as anti-inflammatory signals are triggered by these peptides, and the two formyl peptide receptor (FPR) family members expressed in neutrophils, FPR and FPR-like 1 (FPRL1), have been suggested to transduce these signals. We now report that an annexin AI peptide (Ac9-25) activates, as well as inhibits, the neutrophil release of superoxide anions. Results obtained from experiments with receptor antagonists/inhibitors, desensitized cells, and transfected cells reveal that the Ac9-25 peptide activates the neutrophil reduced nicotinamide adenine dinucleotide phosphate oxidase through FPR but not through FPRL1. The Ac9-25 peptide also inhibits the oxidase activity in neutrophils triggered, not only by the FPR-specific agonist N-formyl-Met-Leu-Phe but also by several other agonists operating through different G protein-coupled receptors. Our data show that the two signals generated by the Ac9-25 peptide are transmitted through different receptors, the inhibitory signal being transduced by a not-yet identified receptor distinct from FPR and FPRL1.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
Medicinska grundvetenskaper ->
Mikrobiologi inom det medicinska området
Annexin A1/immunology, Calcium/metabolism, Cell Differentiation/drug effects, Enzyme Activation/drug effects, HL-60 Cells, Humans, N-Formylmethionine Leucyl-Phenylalanine/pharmacology, NADPH Oxidase/antagonists & inhibitors/*immunology, Neutrophils/drug effects/*enzymology/immunology, Receptors, Formyl Peptide/*antagonists & inhibitors/immunology, Signal Transduction/*drug effects/immunology, Superoxides/antagonists & inhibitors/metabolism, Time Factors
Postens nummer:
Posten skapad:
2007-03-07 17:46
Posten ändrad:
2011-01-20 09:59

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