Oxidative stress and apoptosis in a pig model of brain death (BD) and living donation (LD)
As organ shortage is increasing, the acceptance of marginal donors increases, which might result in poor organ function and patient survival. Mostly, organ damage is caused during brain death (BD), cold ischemic time (CIT) or after reperfusion due to oxidative stress or the induction of apoptosis. T...
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creator | Stiegler, Philipp Sereinigg, Michael Puntschart, Andreas Bradatsch, Andrea Seifert-Held, Thomas Wiederstein-Grasser, Iris Leber, Bettina Stadelmeyer, Elke Dandachi, Nadia Zelzer, Siglinde Iberer, Florian Stadlbauer, Vanessa |
description | As organ shortage is increasing, the acceptance of marginal donors increases, which might result in poor organ function and patient survival. Mostly, organ damage is caused during brain death (BD), cold ischemic time (CIT) or after reperfusion due to oxidative stress or the induction of apoptosis. The aim of this study was to study a panel of genes involved in oxidative stress and apoptosis and compare these findings with immunohistochemistry from a BD and living donation (LD) pig model and after cold ischemia time (CIT).
BD was induced in pigs; after 12 h organ retrieval was performed; heart, liver and kidney tissue specimens were collected in the BD (n = 6) and in a LD model (n = 6). PCR analysis for NFKB1, GSS, SOD2, PPAR-alpha, OXSR1, BAX, BCL2L1, and HSP 70.2 was performed and immunohistochemistry used to show apoptosis and nitrosative stress induced cell damage.
In heart tissue of BD BAX, BCL2L1 and HSP 70.2 increased significantly after CIT. Only SOD2 was over-expressed after CIT in BD liver tissue. In kidney tissue, BCL2L1, NFKB, OXSR1, SOD2 and HSP 70.2 expression was significantly elevated in LD. Immunohistochemistry showed a significant increase in activated Caspase 3 and nitrotyrosine positive cells after CIT in BD in liver and in kidney tissue but not in heart tissue.
The up-regulation of protective and apoptotic genes seems to be divergent in the different organs in the BD and LD setting; however, immunohistochemistry revealed more apoptotic and nitrotyrosine positive cells in the BD setting in liver and kidney tissue whereas in heart tissue both BD and LD showed an increase. |
doi_str_mv | 10.1186/1479-5876-11-244 |
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BD was induced in pigs; after 12 h organ retrieval was performed; heart, liver and kidney tissue specimens were collected in the BD (n = 6) and in a LD model (n = 6). PCR analysis for NFKB1, GSS, SOD2, PPAR-alpha, OXSR1, BAX, BCL2L1, and HSP 70.2 was performed and immunohistochemistry used to show apoptosis and nitrosative stress induced cell damage.
In heart tissue of BD BAX, BCL2L1 and HSP 70.2 increased significantly after CIT. Only SOD2 was over-expressed after CIT in BD liver tissue. In kidney tissue, BCL2L1, NFKB, OXSR1, SOD2 and HSP 70.2 expression was significantly elevated in LD. Immunohistochemistry showed a significant increase in activated Caspase 3 and nitrotyrosine positive cells after CIT in BD in liver and in kidney tissue but not in heart tissue.
The up-regulation of protective and apoptotic genes seems to be divergent in the different organs in the BD and LD setting; however, immunohistochemistry revealed more apoptotic and nitrotyrosine positive cells in the BD setting in liver and kidney tissue whereas in heart tissue both BD and LD showed an increase.</description><identifier>ISSN: 1479-5876</identifier><identifier>EISSN: 1479-5876</identifier><identifier>DOI: 10.1186/1479-5876-11-244</identifier><identifier>PMID: 24088575</identifier><language>eng</language><publisher>England: BioMed Central</publisher><subject>Animals ; Apoptosis ; Apoptosis - genetics ; Biomedical research ; Brain Death - pathology ; Brain research ; Caspase 3 - metabolism ; Catheters ; Disease Models, Animal ; Enzymes ; Experiments ; Gene expression ; Gene Expression Regulation ; Heat shock proteins ; Hepatology ; Hogs ; Immunohistochemistry ; Internal medicine ; Ischemia ; Kidney - metabolism ; Kidney - pathology ; Laboratory animals ; Liver - metabolism ; Liver - pathology ; Mice ; Myocardium - metabolism ; Oxidative stress ; Oxidative Stress - genetics ; Polymerase Chain Reaction ; Rodents ; Surgery ; Sus scrofa</subject><ispartof>Journal of translational medicine, 2013-10, Vol.11 (1), p.244-244</ispartof><rights>2013 Stiegler et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2013 Stiegler et al.; licensee BioMed Central Ltd. 2013 Stiegler et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b550t-dc0c5a244c79511fa163cd656d53292c4d0c4d696b55c111170df4d1e946b2df3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3850531/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3850531/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24088575$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Stiegler, Philipp</creatorcontrib><creatorcontrib>Sereinigg, Michael</creatorcontrib><creatorcontrib>Puntschart, Andreas</creatorcontrib><creatorcontrib>Bradatsch, Andrea</creatorcontrib><creatorcontrib>Seifert-Held, Thomas</creatorcontrib><creatorcontrib>Wiederstein-Grasser, Iris</creatorcontrib><creatorcontrib>Leber, Bettina</creatorcontrib><creatorcontrib>Stadelmeyer, Elke</creatorcontrib><creatorcontrib>Dandachi, Nadia</creatorcontrib><creatorcontrib>Zelzer, Siglinde</creatorcontrib><creatorcontrib>Iberer, Florian</creatorcontrib><creatorcontrib>Stadlbauer, Vanessa</creatorcontrib><title>Oxidative stress and apoptosis in a pig model of brain death (BD) and living donation (LD)</title><title>Journal of translational medicine</title><addtitle>J Transl Med</addtitle><description>As organ shortage is increasing, the acceptance of marginal donors increases, which might result in poor organ function and patient survival. Mostly, organ damage is caused during brain death (BD), cold ischemic time (CIT) or after reperfusion due to oxidative stress or the induction of apoptosis. The aim of this study was to study a panel of genes involved in oxidative stress and apoptosis and compare these findings with immunohistochemistry from a BD and living donation (LD) pig model and after cold ischemia time (CIT).
BD was induced in pigs; after 12 h organ retrieval was performed; heart, liver and kidney tissue specimens were collected in the BD (n = 6) and in a LD model (n = 6). PCR analysis for NFKB1, GSS, SOD2, PPAR-alpha, OXSR1, BAX, BCL2L1, and HSP 70.2 was performed and immunohistochemistry used to show apoptosis and nitrosative stress induced cell damage.
In heart tissue of BD BAX, BCL2L1 and HSP 70.2 increased significantly after CIT. Only SOD2 was over-expressed after CIT in BD liver tissue. In kidney tissue, BCL2L1, NFKB, OXSR1, SOD2 and HSP 70.2 expression was significantly elevated in LD. Immunohistochemistry showed a significant increase in activated Caspase 3 and nitrotyrosine positive cells after CIT in BD in liver and in kidney tissue but not in heart tissue.
The up-regulation of protective and apoptotic genes seems to be divergent in the different organs in the BD and LD setting; however, immunohistochemistry revealed more apoptotic and nitrotyrosine positive cells in the BD setting in liver and kidney tissue whereas in heart tissue both BD and LD showed an increase.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Biomedical research</subject><subject>Brain Death - pathology</subject><subject>Brain research</subject><subject>Caspase 3 - metabolism</subject><subject>Catheters</subject><subject>Disease Models, Animal</subject><subject>Enzymes</subject><subject>Experiments</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Heat shock proteins</subject><subject>Hepatology</subject><subject>Hogs</subject><subject>Immunohistochemistry</subject><subject>Internal medicine</subject><subject>Ischemia</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Laboratory animals</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Mice</subject><subject>Myocardium - metabolism</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - genetics</subject><subject>Polymerase Chain Reaction</subject><subject>Rodents</subject><subject>Surgery</subject><subject>Sus scrofa</subject><issn>1479-5876</issn><issn>1479-5876</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp1kUtLLDEQhYMovveuJOBmXLSmupN-bIR7Z3zBgBvduAnpJD1GupO-Sc-g_96Mo4NeNBASqr46HE4hdATkDKDMz4EWVcLKIk8AkpTSDbS7Lm1--e-gvRCeCUkpo9U22kkpKUtWsF30ePdilBjMQuMweB0CFlZh0bt-cMEEbCwWuDcz3DmlW-waXHsRi0qL4QmP_k5O3wdaszB2hpWzUctZPJpOTg_QViPaoA8_3n30cHV5P75JpnfXt-M_06RmjAyJkkQyEc3LomIAjYA8kypnuWJZWqWSKhJvXuURlxBPQVRDFeiK5nWqmmwfXax0-3ndaSW1Hbxoee9NJ_wrd8Lw7x1rnvjMLXhWMsIyiALjlUBt3C8C3zvSdXyZLV9mywF4dB9VRh82vPs312HgnQlSt62w2s1DHGAVMBJjj-jJf-izm3sbQ4oUTaHMMlJGiqwo6V0IXjdrR0D4cv0_eTj-GsV64HPf2RtEk6nX</recordid><startdate>20131002</startdate><enddate>20131002</enddate><creator>Stiegler, Philipp</creator><creator>Sereinigg, Michael</creator><creator>Puntschart, Andreas</creator><creator>Bradatsch, Andrea</creator><creator>Seifert-Held, Thomas</creator><creator>Wiederstein-Grasser, Iris</creator><creator>Leber, Bettina</creator><creator>Stadelmeyer, Elke</creator><creator>Dandachi, Nadia</creator><creator>Zelzer, Siglinde</creator><creator>Iberer, Florian</creator><creator>Stadlbauer, Vanessa</creator><general>BioMed Central</general><general>BioMed Central Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20131002</creationdate><title>Oxidative stress and apoptosis in a pig model of brain death (BD) and living donation (LD)</title><author>Stiegler, Philipp ; Sereinigg, Michael ; Puntschart, Andreas ; Bradatsch, Andrea ; Seifert-Held, Thomas ; Wiederstein-Grasser, Iris ; Leber, Bettina ; Stadelmeyer, Elke ; Dandachi, Nadia ; Zelzer, Siglinde ; Iberer, Florian ; Stadlbauer, Vanessa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b550t-dc0c5a244c79511fa163cd656d53292c4d0c4d696b55c111170df4d1e946b2df3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Biomedical research</topic><topic>Brain Death - pathology</topic><topic>Brain research</topic><topic>Caspase 3 - metabolism</topic><topic>Catheters</topic><topic>Disease Models, Animal</topic><topic>Enzymes</topic><topic>Experiments</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Heat shock proteins</topic><topic>Hepatology</topic><topic>Hogs</topic><topic>Immunohistochemistry</topic><topic>Internal medicine</topic><topic>Ischemia</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Laboratory animals</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Mice</topic><topic>Myocardium - metabolism</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - genetics</topic><topic>Polymerase Chain Reaction</topic><topic>Rodents</topic><topic>Surgery</topic><topic>Sus scrofa</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Stiegler, Philipp</creatorcontrib><creatorcontrib>Sereinigg, Michael</creatorcontrib><creatorcontrib>Puntschart, Andreas</creatorcontrib><creatorcontrib>Bradatsch, Andrea</creatorcontrib><creatorcontrib>Seifert-Held, Thomas</creatorcontrib><creatorcontrib>Wiederstein-Grasser, Iris</creatorcontrib><creatorcontrib>Leber, Bettina</creatorcontrib><creatorcontrib>Stadelmeyer, Elke</creatorcontrib><creatorcontrib>Dandachi, Nadia</creatorcontrib><creatorcontrib>Zelzer, Siglinde</creatorcontrib><creatorcontrib>Iberer, Florian</creatorcontrib><creatorcontrib>Stadlbauer, Vanessa</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of translational medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Stiegler, Philipp</au><au>Sereinigg, Michael</au><au>Puntschart, Andreas</au><au>Bradatsch, Andrea</au><au>Seifert-Held, Thomas</au><au>Wiederstein-Grasser, Iris</au><au>Leber, Bettina</au><au>Stadelmeyer, Elke</au><au>Dandachi, Nadia</au><au>Zelzer, Siglinde</au><au>Iberer, Florian</au><au>Stadlbauer, Vanessa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxidative stress and apoptosis in a pig model of brain death (BD) and living donation (LD)</atitle><jtitle>Journal of translational medicine</jtitle><addtitle>J Transl Med</addtitle><date>2013-10-02</date><risdate>2013</risdate><volume>11</volume><issue>1</issue><spage>244</spage><epage>244</epage><pages>244-244</pages><issn>1479-5876</issn><eissn>1479-5876</eissn><abstract>As organ shortage is increasing, the acceptance of marginal donors increases, which might result in poor organ function and patient survival. Mostly, organ damage is caused during brain death (BD), cold ischemic time (CIT) or after reperfusion due to oxidative stress or the induction of apoptosis. The aim of this study was to study a panel of genes involved in oxidative stress and apoptosis and compare these findings with immunohistochemistry from a BD and living donation (LD) pig model and after cold ischemia time (CIT).
BD was induced in pigs; after 12 h organ retrieval was performed; heart, liver and kidney tissue specimens were collected in the BD (n = 6) and in a LD model (n = 6). PCR analysis for NFKB1, GSS, SOD2, PPAR-alpha, OXSR1, BAX, BCL2L1, and HSP 70.2 was performed and immunohistochemistry used to show apoptosis and nitrosative stress induced cell damage.
In heart tissue of BD BAX, BCL2L1 and HSP 70.2 increased significantly after CIT. Only SOD2 was over-expressed after CIT in BD liver tissue. In kidney tissue, BCL2L1, NFKB, OXSR1, SOD2 and HSP 70.2 expression was significantly elevated in LD. Immunohistochemistry showed a significant increase in activated Caspase 3 and nitrotyrosine positive cells after CIT in BD in liver and in kidney tissue but not in heart tissue.
The up-regulation of protective and apoptotic genes seems to be divergent in the different organs in the BD and LD setting; however, immunohistochemistry revealed more apoptotic and nitrotyrosine positive cells in the BD setting in liver and kidney tissue whereas in heart tissue both BD and LD showed an increase.</abstract><cop>England</cop><pub>BioMed Central</pub><pmid>24088575</pmid><doi>10.1186/1479-5876-11-244</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Apoptosis Apoptosis - genetics Biomedical research Brain Death - pathology Brain research Caspase 3 - metabolism Catheters Disease Models, Animal Enzymes Experiments Gene expression Gene Expression Regulation Heat shock proteins Hepatology Hogs Immunohistochemistry Internal medicine Ischemia Kidney - metabolism Kidney - pathology Laboratory animals Liver - metabolism Liver - pathology Mice Myocardium - metabolism Oxidative stress Oxidative Stress - genetics Polymerase Chain Reaction Rodents Surgery Sus scrofa |
title | Oxidative stress and apoptosis in a pig model of brain death (BD) and living donation (LD) |
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