NDLI: Heme oxygenase-1 induction contributes to renoprotection by G-CSF during rhabdomyolysis-associated acute kidney injury

Content Provider	PubMed Central
Author	Wei, Qingqing Hill, William D. Su, Yunchao Huang, Shuang Dong, Zheng
Abstract	Granulocyte colony-stimulating factor (G-CSF) is renoprotective during acute kidney injury (AKI) induced by ischemia and cisplatin nephrotoxicity; however, the underlying mechanism is not entirely clear. Rhabdomyolysis is another important clinical cause of AKI, due to the release of nephrotoxins (e.g., heme) from disrupted muscles. The current study has determined the effects of G-CSF on rhabdomyolysis-associated AKI using in vivo and in vitro models. In C57BL/6 mice, intramuscular injection of glycerol induced AKI, which was partially prevented by G-CSF pretreatment. Consistently, glycerol-induced renal tissue damage was ameliorated by G-CSF. In addition, animal survival following the glycerol injection was improved from ∼30 to ∼70% by G-CSF. In cultured renal tubular cells, hemin-induced apoptosis was also suppressed by G-CSF. Interestingly, G-CSF induced heme oxygenase-1 (HO-1, a critical enzyme for heme/hemin degradation and detoxification) in both cultured tubular cells and mouse kidneys. Blockade of HO-1 with protoporphyrin IX zinc(II) (ZnPP) could largely diminish the protective effects of G-CSF. Together, these results demonstrated the renoprotective effects of G-CSF in rhabdomyolysis-associated AKI. Notably, G-CSF may directly protect against tubular cell injury under the disease condition by inducing HO-1.
Related Links	http://dx.doi.org/10.1152/ajprenal.00438.2010
Starting Page	162
File Format	PDF
ISSN	1931857X
e-ISSN	15221466
Journal	American Journal of Physiology - Renal Physiology
Issue Number	1
Volume Number	301
Language	English
Publisher	American Physiological Society
Publisher Date	2011-07-01
Access Restriction	Open
Rights Holder	American Physiological Society
Subject Keyword	Urology Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Urology

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