Genetic variants of the promoter of the heme oxygenase-1 gene and their influence on cardiovascular disease (The Ludwigshafen risk and cardiovascular health study)

Background Heme oxygenase-1 is an inducible cytoprotective enzyme which handles oxidative stress by generating anti-oxidant bilirubin and vasodilating carbon monoxide. A (GT)n dinucleotide repeat and a -413A>T single nuc
Background Heme oxygenase-1 is an inducible cytoprotective enzyme which handles oxidative stress by generating anti-oxidant bilirubin and vasodilating carbon monoxide. A (GT)n dinucleotide repeat and a -413A>T single nucleotide polymorphism have been reported in the promoter region of HMOX1 to both influence the occurrence of coronary artery disease and myocardial infarction. We sought to validate these observations in persons scheduled for coronary angiography. Methods We included 3219 subjects in the current analysis, 2526 with CAD including a subgroup of CAD and MI (n = 1339) and 693 controls. Coronary status was determined by coronary angiography. Risk factors and biochemical parameters (bilirubin, iron, LDL-C, HDL-C, and triglycerides) were determined by standard procedures. The dinucleotide repeat was analysed by PCR and subsequent sizing by capillary electrophoresis, the -413A>T polymorphism by PCR and RFLP. Results In the LURIC study the allele frequency for the -413A>T polymorphism is A = 0,589 and T = 0,411. The (GT)n repeats spread between 14 and 39 repeats with 22 (19.9%) and 29 (47.1%) as the two most common alleles. We found neither an association of the genotypes or allelic frequencies with any of the biochemical parameters nor with CAD or previous MI. Conclusion Although an association of these polymorphisms with the appearance of CAD and MI have been published before, our results strongly argue against a relevant role of the (GT)n repeat or the -413A>T SNP in the HMOX1 promoter in CAD or MI.
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Author:Nicola Lüblinghoff, Karl Winkler, Bernhard Rudolf Winkelmann, Ursula Seelhorst, Britta Wellnitz, Bernhard O. Böhm, Winfried März, Michael Marcus Hoffmann
URN:urn:nbn:de:hebis:30-64253
DOI:http://dx.doi.org/10.1186/1471-2350-10-36
ISSN:1471-2350
Pubmed Id:http://www.ncbi.nlm.nih.gov/pubmed?term=19389234
Parent Title (English):BMC medical genetics
Publisher:BioMed Central ; Springer
Place of publication:London ; Berlin ; Heidelberg
Document Type:Article
Language:English
Date of Publication (online):2009/05/11
Date of first Publication:2009/04/23
Publishing Institution:Universitätsbibliothek Johann Christian Senckenberg
Release Date:2009/05/11
Volume:10
Issue:36
Pagenumber:9
First Page:1
Last Page:9
Note:
© 2009 Lüblinghoff 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.
Source:BMC Medical Genetics 2009, 10:36 ; doi:10.1186/1471-2350-10-36 ; http://www.biomedcentral.com/1471-2350/10/36
HeBIS PPN:212262823
Institutes:Medizin
Dewey Decimal Classification:610 Medizin und Gesundheit
Sammlungen:Universitätspublikationen
Licence (German):License LogoCreative Commons - Namensnennung 2.0

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