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A novel receptor cross-talk between the ATP receptor P2Y2 and formyl peptide receptors reactivates desensitized neutrophils to produce superoxide.

Journal article
Authors Karin Önnheim
Karin Christenson
Michael Gabl
Joachim C Burbiel
Christa E Müller
Tudor I Oprea
Johan Bylund
Claes Dahlgren
Huamei Forsman
Published in Experimental cell research
Volume 323
Issue 1
Pages 209-17
ISSN 1090-2422
Publication year 2014
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Pages 209-17
Language en
Subject categories Basic Medicine


Neutrophils express several G-protein coupled receptors (GPCRs) and they cross regulate each other. We described a novel cross-talk mechanism in neutrophils, by which signals generated by the receptor for ATP (P2Y2) reactivate desensitized formyl peptide receptors (FPRs) so that these ligand-bound inactive FPRs resume signaling. At the signaling level, the cross-talk was unidirectional, i.e., P2Y2 ligation reactivated FPR, but not vice versa and was sensitive to the phosphatase inhibitor calyculinA. Further, we show that the cross talk between P2Y2 and FPR bypassed cytosolic Ca(2+) transients and did not rely on the actin cytoskeleton. In summary, our data demonstrate a novel cross-talk mechanism that results in reactivation of desensitized FPRs and, an amplification of the neutrophil response to ATP.

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