Ischemia-reperfusion induces G-CSF gene expression by renal medullary thick ascending limb cells in vivo and in vitro.
Ischemia-reperfusion induces G-CSF gene expression by renal medullary thick ascending limb cells in vivo and in vitro.
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DOI：
10.1152/ajprenal.00379.2002
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发表时间：
2004-06
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影响因子：
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通讯作者：
Ying Zhang;Vanessa K. Woodward;John M. Shelton;James A. Richardson;Xin J Zhou;D. Link;M. Kielar;D. Rohan Jeyarajah;Christopher Y Lu
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文献类型：
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作者：
Ying Zhang;Vanessa K. Woodward;John M. Shelton;James A. Richardson;Xin J Zhou;D. Link;M. Kielar;D. Rohan Jeyarajah;Christopher Y Lu
缺血性急性肾功能衰竭不仅涉及肾脏，还涉及肾外器官，如产生炎症细胞的骨髓。通过酶联免疫吸附试验和核糖核酸酶保护试验，我们发现肾缺血再灌注后血清中粒细胞巨噬细胞集落刺激因子(G-CSF)蛋白浓度升高，缺血肾组织中G-CSF mRNA和蛋白水平均升高。原位杂交法将G-CSF基因表达增强定位于外髓中的小管细胞，包括髓质厚升肢细胞(MTAL)。我们还发现，体外培养的mTAL在受到活性氧刺激后产生G-CSF蛋白，并增加G-CSF mRNA的表达。肾脏在缺血再灌注后产生G-CSF，为受损肾脏与骨髓之间提供了一种通讯途径。这支持了已知的对缺血的炎症反应。
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.