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NDT Advance Access published online on February 16, 2009
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfp050
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© The Author [2009].
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org


Haematopoietic stem cell migration to the ischemic damaged kidney is not altered by manipulating the SDF-1/CXCR4-axis

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

Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

Correspondence and offprint requests to: Ingrid Stroo, Academic Medical Center, Meibergdreef 9, L2-112, 1105 AZ Amsterdam, The Netherlands. Tel: +31-020-5665715; Fax: +31-020-5669523; E-mail: I.Stroo{at}amc.uva.nl



  Abstract

Background. Haematopoietic stem cells (HSC) have been shown to migrate to the ischemic kidney. The factors that regulate the trafficking of HSC to the ischemic damaged kidney are not fully understood. The stromal cell-derived factor-1 (SDF-1)/CXCR4-axis has been identified as the central signalling axis regulating trafficking of HSC to the bone marrow. Therefore, we hypothesized that SDF-1/CXCR4 interactions are implicated in the migration of HSC to the injured kidney.

Methods. HSC were isolated from mouse bone marrow and labelled with a cell tracker. Acceptor mice were subjected to unilateral ischemia and received HSC intravenously directly after reperfusion. In addition, in separate groups of acceptor mice, endogenous SDF-1 or HSC-associated CXCR4 was blocked or kidneys were injected with SDF-1.

Results. Exogenous HSC could be detected in the tubules and interstitium of the kidney 24 h after ischemic injury. Importantly, the amount of HSC in the ischemic kidney was markedly higher compared to the contralateral kidney. Neutralizing endogenous SDF-1 or HSC-associated CXCR4 did not prevent the migration of HSC. No increase in the number of labelled HSC could be observed after local administration of SDF-1, as was also determined in bilateral kidney ischemia.

Conclusion. In conclusion, systemically administered HSC preferentially migrate to the ischemic injured kidney. This migration could not be prevented by blocking the SDF-1/CXCR4-axis or increased after local administration of SDF-1.

Keywords: HSC migration; ischemia/reperfusion; kidney; SDF-1/CXCR4-axis

* These authors contributed equally to this study.

Received for publication: 16. 9.08
Accepted in revised form: 23. 1.09


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