ArticleJournal of translational medicine2013
Brain death induces renal expression of heme oxygenase-1 and heat shock protein 70.
Article in Journal of translational medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Heme-Oxygenase and Kidney Transplantation: A Potential for Target Therapy?Biomolecules · 2020Review
- Inadequate Antioxidative Responses in Kidneys of Brain-Dead Rats.Transplantation · 2017Article
- Heatstroke Effect on Brain Heme Oxygenase-1 in Rats.International journal of medical sciences · 2015Article
- Oxidative stress and apoptosis in a pig model of brain death (BD) and living donation (LD).Journal of translational medicine · 2013Article
- Increased resistin in brain dead organ donors is associated with delayed graft function after kidney transplantation.Journal of translational medicine · 2013Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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