Brain death induces renal expression of heme oxygenase-1 and heat shock protein 70

Journal of Translational Medicine

Research

Rutger J Ploeg¹  Henri GD Leuvenink¹  Theo A Schuurs¹  Leon FA van Dullemen¹  Harry van Goor²  Eelke M Bos²  Harm H Kampinga³ 

[1] Departments of Surgery, University Medical Center Groningen, University of Groningen, PO Box 30.001, Hanzeplein 1, 9700 RB, Groningen, The Netherlands;Pathology and Laboratory Medicine, University Medical Center Groningen, University of Groningen, PO Box 30.001, Hanzeplein 1, 9700 RB, Groningen, The Netherlands;Radiation and Stress Cell Biology, University Medical Center Groningen, University of Groningen, PO Box 30.001, Hanzeplein 1, 9700 RB, Groningen, The Netherlands;

关键词: Kidney;    Protective genes;    Rat;    Organ donation;    HSP;    HSP70;    HSP40;    HSP27;   

DOI  :  10.1186/1479-5876-11-22

 received in 2012-09-26, accepted in 2013-01-25,  发布年份 2013

来源: Springer

【 摘 要 】

BackgroundKidneys derived from brain dead donors have lower graft survival and higher graft-function loss compared to their living donor counterpart. Heat Shock Proteins (HSP) are a large family of stress proteins involved in maintaining cell homeostasis. We studied the role of stress-inducible genes Heme Oxygenase-1 (HO-1), HSP27, HSP40, and HSP70 in the kidney following a 4 hour period of brain death.MethodsBrain death was induced in rats (n=6) by inflating a balloon catheter in the epidural space. Kidneys were analysed for HSPs using RT-PCR, Western blotting, and immunohistochemistry.ResultsRT-PCR data showed a significant increase in gene expression for HO-1 and HSP70 in kidneys of brain dead rats. Western blotting revealed a massive increase in HO-1 protein in brain dead rat kidneys. Immunohistochemistry confirmed these findings, showing extensive HO-1 protein expression in the renal cortical tubules of brain dead rats. HSP70 protein was predominantly increased in renal distal tubules of brain dead rats treated for hypotension.ConclusionRenal stress caused by brain death induces expression of the cytoprotective genes HO-1 and HSP70, but not of HSP27 and HSP40. The upregulation of these cytoprotective genes indicate that renal damage occurs during brain death, and could be part of a protective or recuperative mechanism induced by brain death-associated stress.

【 授权许可】

CC BY   
© van Dullemen et al.; licensee BioMed Central Ltd. 2013