Association of Functional Heme Oxygenase‐1 Gene Promoter Polymorphism with Renal Transplantation Outcomes
Heme oxygenase‐1 (HO‐1) is a cytoprotective molecule and increased expression in experimental transplant models correlates with reduced graft injury. A functional dinucleotide repeat (GT)n polymorphism, within the HO‐1 promoter, regulates gene expression; a short number of repeats (S‐allele
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| Veröffentlicht in: | American journal of transplantation 2007-04, Vol.7 (4), p.908-913 |
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| container_title | American journal of transplantation |
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| creator | Courtney, A. E. McNamee, P. T. Middleton, D. Heggarty, S. Patterson, C. C. Maxwell, A. P. |
| description | Heme oxygenase‐1 (HO‐1) is a cytoprotective molecule and increased expression in experimental transplant models correlates with reduced graft injury. A functional dinucleotide repeat (GT)n polymorphism, within the HO‐1 promoter, regulates gene expression; a short number of repeats (S‐allele |
| doi_str_mv | 10.1111/j.1600-6143.2006.01726.x |
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The graft and recipient survival of 707 first deceased donor renal transplants was not significantly influenced by the (GT)n length polymorphism of the HO‐1 gene promoter.</description><identifier>ISSN: 1600-6135</identifier><identifier>EISSN: 1600-6143</identifier><identifier>DOI: 10.1111/j.1600-6143.2006.01726.x</identifier><identifier>PMID: 17391133</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult ; Biological and medical sciences ; Cadaver ; Dinucleotide Repeats - genetics ; DNA - genetics ; DNA - isolation & purification ; Female ; Genotype ; Graft Survival - physiology ; Heme oxygenase ; Heme Oxygenase-1 - genetics ; Humans ; kidney transplantation ; Kidney Transplantation - mortality ; Kidney Transplantation - physiology ; Male ; Medical sciences ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Prevention and actions ; Promoter Regions, Genetic ; protective genes ; Public health. Hygiene ; Public health. Hygiene-occupational medicine ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the urinary system ; Survival Analysis ; Tissue Donors ; transplant outcomes ; Treatment Outcome</subject><ispartof>American journal of transplantation, 2007-04, Vol.7 (4), p.908-913</ispartof><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4786-fede25d26c6db2aa42702153e35c23410d01b3135095108f2628a17fc1ab5b5d3</citedby><cites>FETCH-LOGICAL-c4786-fede25d26c6db2aa42702153e35c23410d01b3135095108f2628a17fc1ab5b5d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1600-6143.2006.01726.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1600-6143.2006.01726.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18701500$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17391133$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Courtney, A. E.</creatorcontrib><creatorcontrib>McNamee, P. T.</creatorcontrib><creatorcontrib>Middleton, D.</creatorcontrib><creatorcontrib>Heggarty, S.</creatorcontrib><creatorcontrib>Patterson, C. C.</creatorcontrib><creatorcontrib>Maxwell, A. P.</creatorcontrib><title>Association of Functional Heme Oxygenase‐1 Gene Promoter Polymorphism with Renal Transplantation Outcomes</title><title>American journal of transplantation</title><addtitle>Am J Transplant</addtitle><description>Heme oxygenase‐1 (HO‐1) is a cytoprotective molecule and increased expression in experimental transplant models correlates with reduced graft injury. A functional dinucleotide repeat (GT)n polymorphism, within the HO‐1 promoter, regulates gene expression; a short number of repeats (S‐allele <25) increases transcription. The role of this HO‐1 gene promoter polymorphism on renal transplant outcomes was assessed. DNA from 707 donor/recipient pairs (n = 1414) of first deceased donor renal transplants (99% Caucasian) was genotyped. Graft survival was not significantly impacted by carriage of an S‐allele by the donor (hazard ratio 0.89, 95% CI 0.71–1.11; p = 0.28) or recipient (hazard ratio 1.19, 95% CI 0.95–1.48; p = 0.13). Similarly neither donor nor recipient genotype influenced recipient survival (hazard ratio 0.89, 95% CI 0.67–1.18; p = 0.41, and hazard ratio 1.22, 95% CI 0.93–1.62; p = 0.16). The hazard ratios changed only minimally in multivariate analysis including significant survival factors. Genotype did not alter the incidence of acute rejection or chronic allograft nephropathy. There is no evidence of a protective effect for the S‐allele of the HO‐1 gene promoter polymorphism on graft or recipient survival in clinical renal transplantation.
The graft and recipient survival of 707 first deceased donor renal transplants was not significantly influenced by the (GT)n length polymorphism of the HO‐1 gene promoter.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Cadaver</subject><subject>Dinucleotide Repeats - genetics</subject><subject>DNA - genetics</subject><subject>DNA - isolation & purification</subject><subject>Female</subject><subject>Genotype</subject><subject>Graft Survival - physiology</subject><subject>Heme oxygenase</subject><subject>Heme Oxygenase-1 - genetics</subject><subject>Humans</subject><subject>kidney transplantation</subject><subject>Kidney Transplantation - mortality</subject><subject>Kidney Transplantation - physiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Polymerase Chain Reaction</subject><subject>Polymorphism, Genetic</subject><subject>Prevention and actions</subject><subject>Promoter Regions, Genetic</subject><subject>protective genes</subject><subject>Public health. Hygiene</subject><subject>Public health. Hygiene-occupational medicine</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Surgery of the urinary system</subject><subject>Survival Analysis</subject><subject>Tissue Donors</subject><subject>transplant outcomes</subject><subject>Treatment Outcome</subject><issn>1600-6135</issn><issn>1600-6143</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1u2zAQhYmiRfPTXiHgpt1ZnSFNSl50YQT5KwI4CNw1QVGjRo4kOqSE2LseoWfMSSLVRrJMuOEA_N7M8D3GOEKCw_mxSlADTDROZSIAdAKYCp1sPrDDl4ePL7VUB-woxhWMVCY-swNM5QxRykN2P4_Ru8p2lW-5L_l537qxtjW_pIb4YrP9Q62N9PT3H_ILaonfBN_4jgK_8fW28WF9V8WGP1bdHb-lUbgMto3r2rbdru2i75xvKH5hn0pbR_q6v4_Z7_Oz5enl5HpxcXU6v564aZrpSUkFCVUI7XSRC2unIgWBSpJUTsgpQgGYy-FXMFMIWSm0yCympUObq1wV8ph93_VdB__QU-xMU0VH9bAR-T6aFCQqVOJNUCAoDTMcwGwHuuBjDFSadagaG7YGwYyJmJUZzTaj8WZMxPxPxGwG6cl-Rp83VLwK9xEMwLc9YKOzdTmY56r4ymUpoAIYuJ877rGqafvuBcz813Ks5DPg5ae6</recordid><startdate>200704</startdate><enddate>200704</enddate><creator>Courtney, A. E.</creator><creator>McNamee, P. T.</creator><creator>Middleton, D.</creator><creator>Heggarty, S.</creator><creator>Patterson, C. C.</creator><creator>Maxwell, A. P.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>IQODW</scope><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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>200704</creationdate><title>Association of Functional Heme Oxygenase‐1 Gene Promoter Polymorphism with Renal Transplantation Outcomes</title><author>Courtney, A. E. ; McNamee, P. T. ; Middleton, D. ; Heggarty, S. ; Patterson, C. C. ; Maxwell, A. P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4786-fede25d26c6db2aa42702153e35c23410d01b3135095108f2628a17fc1ab5b5d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Cadaver</topic><topic>Dinucleotide Repeats - genetics</topic><topic>DNA - genetics</topic><topic>DNA - isolation & purification</topic><topic>Female</topic><topic>Genotype</topic><topic>Graft Survival - physiology</topic><topic>Heme oxygenase</topic><topic>Heme Oxygenase-1 - genetics</topic><topic>Humans</topic><topic>kidney transplantation</topic><topic>Kidney Transplantation - mortality</topic><topic>Kidney Transplantation - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Polymerase Chain Reaction</topic><topic>Polymorphism, Genetic</topic><topic>Prevention and actions</topic><topic>Promoter Regions, Genetic</topic><topic>protective genes</topic><topic>Public health. Hygiene</topic><topic>Public health. Hygiene-occupational medicine</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Surgery of the urinary system</topic><topic>Survival Analysis</topic><topic>Tissue Donors</topic><topic>transplant outcomes</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Courtney, A. E.</creatorcontrib><creatorcontrib>McNamee, P. T.</creatorcontrib><creatorcontrib>Middleton, D.</creatorcontrib><creatorcontrib>Heggarty, S.</creatorcontrib><creatorcontrib>Patterson, C. C.</creatorcontrib><creatorcontrib>Maxwell, A. P.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Courtney, A. E.</au><au>McNamee, P. T.</au><au>Middleton, D.</au><au>Heggarty, S.</au><au>Patterson, C. C.</au><au>Maxwell, A. P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of Functional Heme Oxygenase‐1 Gene Promoter Polymorphism with Renal Transplantation Outcomes</atitle><jtitle>American journal of transplantation</jtitle><addtitle>Am J Transplant</addtitle><date>2007-04</date><risdate>2007</risdate><volume>7</volume><issue>4</issue><spage>908</spage><epage>913</epage><pages>908-913</pages><issn>1600-6135</issn><eissn>1600-6143</eissn><abstract>Heme oxygenase‐1 (HO‐1) is a cytoprotective molecule and increased expression in experimental transplant models correlates with reduced graft injury. A functional dinucleotide repeat (GT)n polymorphism, within the HO‐1 promoter, regulates gene expression; a short number of repeats (S‐allele <25) increases transcription. The role of this HO‐1 gene promoter polymorphism on renal transplant outcomes was assessed. DNA from 707 donor/recipient pairs (n = 1414) of first deceased donor renal transplants (99% Caucasian) was genotyped. Graft survival was not significantly impacted by carriage of an S‐allele by the donor (hazard ratio 0.89, 95% CI 0.71–1.11; p = 0.28) or recipient (hazard ratio 1.19, 95% CI 0.95–1.48; p = 0.13). Similarly neither donor nor recipient genotype influenced recipient survival (hazard ratio 0.89, 95% CI 0.67–1.18; p = 0.41, and hazard ratio 1.22, 95% CI 0.93–1.62; p = 0.16). The hazard ratios changed only minimally in multivariate analysis including significant survival factors. Genotype did not alter the incidence of acute rejection or chronic allograft nephropathy. There is no evidence of a protective effect for the S‐allele of the HO‐1 gene promoter polymorphism on graft or recipient survival in clinical renal transplantation.
The graft and recipient survival of 707 first deceased donor renal transplants was not significantly influenced by the (GT)n length polymorphism of the HO‐1 gene promoter.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>17391133</pmid><doi>10.1111/j.1600-6143.2006.01726.x</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Biological and medical sciences Cadaver Dinucleotide Repeats - genetics DNA - genetics DNA - isolation & purification Female Genotype Graft Survival - physiology Heme oxygenase Heme Oxygenase-1 - genetics Humans kidney transplantation Kidney Transplantation - mortality Kidney Transplantation - physiology Male Medical sciences Polymerase Chain Reaction Polymorphism, Genetic Prevention and actions Promoter Regions, Genetic protective genes Public health. Hygiene Public health. Hygiene-occupational medicine Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the urinary system Survival Analysis Tissue Donors transplant outcomes Treatment Outcome |
| title | Association of Functional Heme Oxygenase‐1 Gene Promoter Polymorphism with Renal Transplantation Outcomes |
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