SDF-1 provides morphological and functional protection against renal ischaemia/reperfusion injury

The chemokine stromal cell-derived factor-1 (SDF-1) is thought to be involved in mediating tissue repair by promoting migration of bone marrow stem or progenitor cells to the site of injury. Increased levels of renal SDF-1 are found after kidney injury. However, recently, we showed that SDF-1 does n...

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Vydané v:	Nephrology, dialysis, transplantation Ročník 25; číslo 12; s. 3852
Hlavní autori:	Stokman, Geurt, Stroo, Ingrid, Claessen, Nike, Teske, Gwendoline J D, Florquin, Sandrine, Leemans, Jaklien C
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	England 01.12.2010
Predmet:	Acute Kidney Injury - metabolism Acute Kidney Injury - pathology Acute Kidney Injury - prevention & control Animals Apoptosis - drug effects Cell Movement - physiology Chemokine CXCL12 - antagonists & inhibitors Chemokine CXCL12 - drug effects Chemokine CXCL12 - metabolism Hematopoietic Stem Cells - cytology Hematopoietic Stem Cells - physiology Kidney Cortex - drug effects Kidney Cortex - metabolism Kidney Cortex - pathology Kidney Medulla - drug effects Kidney Medulla - metabolism Kidney Medulla - pathology Male Mice Mice, Inbred C57BL Models, Animal Oligonucleotides, Antisense - pharmacology Reperfusion Injury - metabolism Reperfusion Injury - pathology Reperfusion Injury - prevention & control Signal Transduction - physiology
ISSN:	1460-2385, 1460-2385
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Shrnutí:	The chemokine stromal cell-derived factor-1 (SDF-1) is thought to be involved in mediating tissue repair by promoting migration of bone marrow stem or progenitor cells to the site of injury. Increased levels of renal SDF-1 are found after kidney injury. However, recently, we showed that SDF-1 does not play an important role in the migration of haematopoietic stem cells to the post-ischaemic kidney. The function of increased post-ischaemic renal SDF-1 expression in modulating renal ischaemia/reperfusion injury remains, therefore, unknown. We studied the role of SDF-1 in renal ischaemia/reperfusion injury by locally decreasing SDF-1 expression and subsequent SDF-1 signalling in the corticomedullary region of the kidney using antisense oligonucleotide treatment in mice. Renal SDF-1 protein increased significantly in the early phase of ischaemia/reperfusion injury. Antisense treatment resulted in a reduction of corticomedullary SDF-1 expression which was accompanied by severely increased tubular injury and decreased renal function. We did not observe any difference in mobilization or retention of CXCR4-positive haematopoietic stem or progenitor cells after induction of renal ischaemia. Rather, antisense-treated animals showed markedly increased apoptosis of the tubular epithelium accompanied by an increased renal inflammatory response. Conclusions. These data indicate a new role for SDF-1 in renal pathogenesis by mediating tubular epithelial protection against ischaemic injury and suggest that SDF-1 by itself is not crucial for the influx of haematopoietic stem or progenitor cells towards the ischaemic injured kidney.
Bibliografia:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1460-2385 1460-2385
DOI:	10.1093/ndt/gfq311