Heme Oxygenase-1 Gene Promoter Microsatellite Polymorphism is Associated with Restenosis after Percutaneous Transluminal Angioplasty

Exner, Markus; Schillinger, Martin; Minar, Erich; Mlekusch, Wolfgang; Schlerka, Gerald; Haumer, Markus; Mannhalter, Christine; Wagner, Oswald

doi:10.1177/152660280100800501

Cited by 144 publications

(134 citation statements)

References 39 publications

Supporting

Mentioning

129

Contrasting

Unclassified

Order By: Relevance

“…The distribution of the (GT)n repeat alleles was bimodal, with one peak at allele 23 and the other at allele 30, similar as reported in other literatures [7,10]. Based on this observation, a previous description [11], and because the number of repeats was inversely correlated to HO-1 production and activity, we divided the alleles into two subclasses, one with ≤25 repeats (the short (S) class) and one with >25 repeats (the long (L) class). The HO-1 genotype was composed of a combination of S-and/or L-alleles with genotypes SS, SL, and LL.…”

Section: Ho-1 Genotype Distribution In the Recipients And Donorssupporting

confidence: 75%

Heme Oxygenase-1 Promoter Polymorphism Protects Liver Allograft

Zhang

Guan

et al. 2015

Indian J Surg

View full text Add to dashboard Cite

Heme oxygenase-1 has been identified to protect allograft from ischemia/reperfusion and immunologic rejection. Activity of heme oxygenase-1 is regulated by a guanine-thymine dinucleotide length polymorphism in the heme oxygenase-1 gene promoter. In this study, we aimed to explore the impact of the heme oxygenase-1 gene promoter polymorphism of donors and recipients on the orthotopic liver graft function after transplantation. Sixty recipients and their accompanying donors of orthotopic liver allografts were included retrospectively in this study. Heme oxygenase-1 gene promoter polymorphism was assessed using genomic DNA isolated from cryopreserved splenocytes or peripheral blood mononuclear cells and analyzed by genetic analyzer. Small allele of the donor heme oxygenase-1 gene polymorphism significantly prolonged the graft survival (p=0.017). Recipients of allografts from a class of small-allele carrier had significantly lower serum total bilirubin compared with recipients of a nonclass small-allele donor liver (p < 0.01).Additionally, in recipients of small-carrier allografts, cold ischemia time (<10 h or ≥10 h) did not affect the total bilirubin significantly. Our study suggested a protective function of donor-derived heme oxygenase-1 gene promoter polymorphism on orthotopic liver allograft function after transplantation.

show abstract

Section: Ho-1 Genotype Distribution In the Recipients And Donorssupporting

confidence: 75%

Heme Oxygenase-1 Promoter Polymorphism Protects Liver Allograft

Zhang

Guan

et al. 2015

Indian J Surg

View full text Add to dashboard Cite

show abstract

“…thors have described a microsatellite polymorphism in the HO-1 promoter (a small number of GT repeats in the promoter region responsible for a higher HO activity) in humans that is associated with a reduced susceptibility to coronary disease (42) or restenosis after angioplasty (43). In these studies, the anti-oxidant role of HO has been advocated to explain its protective effect, but an interaction with the oxidase function has never been postulated.…”

Section: Discussionmentioning

confidence: 99%

Induction of Heme Oxygenase-1 Inhibits NAD(P)H Oxidase Activity by Down-regulating Cytochrome b558 Expression via the Reduction of Heme Availability

Taillé

El-Benna²,

Lanone

et al. 2004

Journal of Biological Chemistry

168

107

View full text Add to dashboard Cite

Heme-oxygenase-1 (HO-1), the rate-limiting enzyme of heme degradation, has powerful anti-oxidant properties related to the production of the reactive oxygen species scavenger bilirubin. However, some data suggest that HO-1 could also inhibit the cellular production of reactive oxygen species. Therefore, we investigated whether the anti-oxidant properties of HO-1 could be mediated by modulation of the activity and/or expression of the heme-containing NAD(P)H oxidase, the main source of the superoxide anion ( . production and gp91 phox expression induced by HO-1 overexpression. Similar results were obtained in vivo in rat alveolar macrophages after pharmacological modulation of HO-1 expression or activity. These results show that a decrease in heme content due to HO-1 activation limits heme availability for maturation of the gp91 phox subunit and assembly of the functional NAD(P)H oxidase. This study provides a new mechanism to explain HO-1 anti-oxidant properties.

show abstract

“…On this basis, we divided HO-1 (GT) n alleles into 2 categories: short (S) alleles (Յ25 GT repeats) and long (L) alleles (Ͼ25 GT repeats). This classification criterion has been commonly applied in previous HO-1 association and functional studies (14,16,18,19).…”

Section: Resultsmentioning

confidence: 99%

HO‐1 promoter polymorphism associated with rheumatoid arthritis

Rueda

Oliver

Robledo

et al. 2007

Arthritis & Rheumatism

View full text Add to dashboard Cite

Objective. To investigate the role of the HO-1 gene as a novel functional candidate gene for rheumatoid arthritis (RA).Methods. We performed a case-control study including 736 RA patients and 846 healthy controls of Spanish Caucasian origin. Two putative functional HO-1 promoter polymorphisms, a (GT) n microsatellite and a -413 A/T single-nucleotide polymorphism (SNP), were selected as genetic markers and genotyped using polymerase chain reaction-based methods. In addition, the intracellular expression of heme oxygenase 1 (HO-1) was determined in healthy individuals with different (GT) n genotypes.Results. The distribution of HO-1 (GT) n short (S) alleles (<25 GT repeats) and long (L) alleles (>25 GT repeats) revealed a significant protective effect of S (GT) n alleles (P ‫؍‬ 0.019) (odds ratio [OR] 0.8, 95% confidence interval [95% CI] 0.7-0.9) and the SS (GT) n genotype (P ‫؍‬ 0.002) (OR 0.6, 95% CI 0.4-0.9). In contrast, the -413 HO-1 promoter SNP did not yield any statistically significant deviation between RA patients and controls, considering either allele or genotype frequencies. The haplotype analysis showed a strong protective effect of the S/A haplotype (P ‫؍‬ 7 ؋ 10 ؊7 , corrected P [P corr ] ‫؍‬ 3 ؋ 10 ؊6 ) (OR 0.4, 95% CI 0.3-0.6), whereas the L/A haplotype showed the opposite tendency (P ‫؍‬ 0.008, P corr ‫؍‬ 0.03) (OR 1.2, 95% CI 1.0-1.4). In addition, we demonstrated that monocytes from individuals carrying the SS (GT) n genotype showed a significantly higher percentage of HO-1 expression than did cells from LL homozygous individuals (P ‫؍‬ 0.0003). Conclusion. In this study, we identified the HO-1 (GT) n microsatellite as a new genetic marker involved in RA genetics in our population.

show abstract

Heme Oxygenase-1 Gene Promoter Microsatellite Polymorphism is Associated with Restenosis after Percutaneous Transluminal Angioplasty

Cited by 144 publications

References 39 publications

Heme Oxygenase-1 Promoter Polymorphism Protects Liver Allograft

Heme Oxygenase-1 Promoter Polymorphism Protects Liver Allograft

Induction of Heme Oxygenase-1 Inhibits NAD(P)H Oxidase Activity by Down-regulating Cytochrome b558 Expression via the Reduction of Heme Availability

HO‐1 promoter polymorphism associated with rheumatoid arthritis

Contact Info

Product

Resources

About