期刊
EXPERIMENTAL CELL RESEARCH
卷 323, 期 1, 页码 209-217出版社
ELSEVIER INC
DOI: 10.1016/j.yexcr.2014.01.023
关键词
ATP; Formyl peptides; G-protein coupled receptors; Cross-talk; Neutrophils
资金
- Swedish Medical Research Council
- King Gustaf V 80-Year Foundation
- Goteborg Rheumatism Association
- Ingabritt and Arne Lundber foundation
- Swedish state under the ALF-agreement
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 (P2Y(2)) 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., P2Y(2) ligation reactivated FPR, but not vice versa and was sensitive to the phosphatase inhibitor calyculinA. Further, we show that the cross talk between P2Y(2) and FPR bypassed cytosolic Ca2+ 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. (C) 2014 Elsevier Inc All rights reserved.
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