Journal
JOURNAL OF PATHOLOGY
Volume 225, Issue 4, Pages 597-608Publisher
WILEY-BLACKWELL
DOI: 10.1002/path.2982
Keywords
tissue repair; inflammation; FTY720; lipid signalling; ischaemia/reperfusion; NGAL; regeneration
Funding
- Deutsche Forschungsgemeinschaft [BR999, ECCPS, SFB815]
- Sander Foundation
- Deutsche Krebshilfe
- LOEWE (LiFF)
- National Spanish Research Actions [FIS 05/0156, FIS 06/0173]
- EU (PROLIGEN)
- IDIBAPS
- Fritz-Thyssen-Stiftung
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Inflammatory reactions are initiated to eliminate pathogens, but also to promote repair of damaged tissue after acute inflammation is terminated. In this regard, macrophages play a prominent role during induction as well as resolution of inflammation and injury in various organs including the kidney. The present study describes a mechanism for renal tissue regeneration after ischaemia/reperfusion injury. Following injury, apoptotic cell-derived sphingosine-1-phosphate (S1P) or exogenously administered sphingosine analogue FTY720 activates macrophages to support the proliferation and healing of renal epithelium, once inflammatory conditions are terminated. Both suppression of inflammation and renal regeneration might require S1P receptor 3 (S1P3) signalling and downstream release of neutrophil gelatinase-associated lipocalin (NGAL/Lcn-2) from macrophages. Overall, our data point to a macrophage-dependent S1P-S1P3-Lcn-2 axis that might be beneficial for restoration of kidney function after an ischaemic insult. Copyright (C) 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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