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Am J Physiol Renal Physiol 286: F1193-F1201, 2004. First published January 20, 2004; doi:10.1152/ajprenal.00379.2002
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Ischemia-reperfusion induces G-CSF gene expression by renal medullary thick ascending limb cells in vivo and in vitro

Ying Zhang,1 Vanessa K. Woodward,1 John M. Shelton,2 James A. Richardson,3 Xin J. Zhou,3 Daniel Link,4 Mariusz L. Kielar,1 D. Rohan Jeyarajah,5 and Christopher Y. Lu1,6

1 Internal Medicine (Nephrology), 2Internal Medicine (Cardiology), 3Pathology and Molecular Biology, and 5Surgery, and 6Graduate Program in Immunology, University of Texas Southwestern Medical Center, Dallas, Texas 75390; and 4Department of Medicine, Washington University School of Medicine, St. Louis, Missouri

Submitted 21 October 2002 ; accepted in final form 9 January 2004

Ischemic acute renal failure involves not only the kidney but also extrarenal organs such as the bone marrow that produces inflammatory cells. By ELISA and RNase protection assays, we now show that renal ischemia-reperfusion increases serum concentrations of granulocyte macrophage colony-stimulating factor (G-CSF) protein and increases both G-CSF mRNA and protein in the ischemic kidney. In situ hybridization localized the increased G-CSF mRNA to tubule cells, including medullary thick ascending limb cells (mTAL), in the outer medulla. We also show that mTAL produce G-CSF protein and increase G-CSF mRNA after stimulation by reactive oxygen species in vitro. The production of G-CSF by the kidney after ischemia-reperfusion provides a means of communication from the injured kidney to the bone marrow. This supports the known inflammatory response to ischemia.

acute renal failure; ischemia; granulocyte colony-stimulating factor; reactive oxygen species; medullary thick ascending limb tubules


Address for reprint requests and other correspondence: C. Y. Lu, Div. of Nephrology (Internal Medicine), Univ. of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390–8856 (E-mail: christopher.lu{at}utsouthwestern.edu).




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