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

Authors: Van Dullemen, LF  Bos, EM  Schuurs, TA  Kampinga, HH  Ploeg, RJ  Van Goor, H  Leuvenink, HG 
Citation: van Dullemen LF, etal., J Transl Med. 2013 Jan 29;11:22. doi: 10.1186/1479-5876-11-22.
Pubmed: (View Article at PubMed) PMID:23356498
DOI: Full-text: DOI:10.1186/1479-5876-11-22

BACKGROUND: Kidneys 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. METHODS: Brain 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. RESULTS: RT-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. CONCLUSION: Renal 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.

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CRRD ID: 10755728
Created: 2016-02-03
Species: All species
Last Modified: 2016-02-03
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.