Journal Article

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

Geurt Stokman, Ingrid Stroo, Nike Claessen, Gwendoline J.D. Teske, Sandrine Florquin and Jaklien C. Leemans

in Nephrology Dialysis Transplantation

Published on behalf of European Renal Association - European Dialysis and Transplant Assoc

Volume 25, issue 12, pages 3852-3859
Published in print December 2010 | ISSN: 0931-0509
Published online June 2010 | e-ISSN: 1460-2385 | DOI: https://dx.doi.org/10.1093/ndt/gfq311
SDF-1 provides morphological and functional protection against renal ischaemia/reperfusion injury

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Background. 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.

Methods. 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.

Results. 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.

Keywords: apoptosis; ischaemia/reperfusion; SDF-1; tubular epithelial cells

Journal Article.  4315 words.  Illustrated.

Subjects: Nephrology

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