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Am J Physiol Renal Physiol (January 20, 2004). doi:10.1152/ajprenal.00379.2002
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Submitted on October 21, 2002
Accepted on January 9, 2004

Ischemia/ reperfusion induces G-CSF gene expression by renal medullary thick ascending limb cells in vivo and in vitro

Ying Zhang1, Vanessa K. Woodward1, John M. Shelton2, James A. Richardson3, Xin Ji Zhou3, Daniel Link4, Mariusz L. Kielar1, D. Rohan Jeyarajah5, and Christopher Y. Lu6*

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

* To whom correspondence should be addressed. E-mail: christopher.lu{at}utsouthwestern.edu.

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 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 (ROS) 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.




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