Association of the glutathione S-transferase M1 homozygous null genotype with susceptibility to Sj�gren's syndrome in Japanese individuals

Morinobu, Akio; Kanagawa, Sugayo; Koshiba, Masanori; Sugai, Susumu; Kumagai, Shunichi

doi:10.1002/1529-0131(199912)42:12<2612::aid-anr15>3.0.co;2-v

Cited by 36 publications

(18 citation statements)

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“…Worldwide differences in GSTT1 frequencies were previously documented [10,12], with 20% of Caucasians, 60% of Asians and 40% of Africans not expressing the GSTT1 enzyme [5]. The frequencies of GSTT1 deletion in our populations were higher than that described for Europeans, including British (18%) [20], French (16%) [21], German (13%) [22] and Austrian (20%) [23], as well as for other Middle Eastern populations, including Turks (17.3%) [24], and Iranians (21.2%) [25], but was significantly lower than SouthEast Asians, such as Chinese (56.5%) [26], Koreans (53.8%) [27] and Japanese (44%) [28]. The frequencies of GSTT1 null genotype in our Arab populations are similar to that of the sub-Saharan Africans: Zimbabweans (26%) [30], Gambians (37.1%) [31], Cameroonians (46.8%) [32] and Ivory Coast (33.1%) [33] (Table 2).…”

Section: Discussionmentioning

confidence: 67%

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Genetic Polymorphism of the Glutathione S-Transferase M1 and T1 Genes in Three Distinct Arab Populations

et al. 2011

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Abstract. Deletion polymorphisms for the glutathione S-transferase (GST) gene are associated with increased risk of cancer, and are implicated in detoxifying mutagenic electrophilic compounds. GST Polymorphic variants were reported for different populations. The aim of this study was to investigate the frequencies of GSTM1 and GSTT1 null genotypes among Bahraini, Lebanese and Tunisian Arabs. GST genotyping was done by multiplex PCR-based methods. Study subjects comprised 167 Bahrainis, 141 Lebanese and 186 Tunisians unrelated healthy individuals. GSTM1 deletion homozygosity of 49.7%, 52.5% and 63.4% were recorded for Bahraini, Lebanese and Tunisians, respectively. Among Bahrainis, the prevalence of GSTT1 null homozygotes was 28.7%, while in higher rates were seen in Lebanese (37.6%) and Tunisians (37.1%). Our results indicate that there are no major differences in allelic distribution of GSTM1 and GSTT1 genes between the three Arab populations investigated except between Bahrainis and Tunisians regarding the allelic distribution of GSTM1 gene (P = 0.013). Combined analysis of both genes revealed that 14.4% of Bahrainis, 16.3% of Lebanese and 21.0% of Tunisians harbor the deleted genotype of both genes. This is the first study that addresses GST gene polymorphism in Bahraini and Lebanese Arabs, and will help genetic studies on the association of GSTM1 and GSTT1 polymorphisms with disease risks and drug effects in Arab populations.

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Section: Discussionmentioning

confidence: 67%

“…(53%) [27] and Japanese (44%) [28] (Table 2). Significant differences in GSTM1 null genotype distribution were seen with respect to Indians (20.7%) [29], and Africans, including Zimbabweans (24%) [30], Gambians (20.2%) [31], Cameroonians (27.8%) [32], and Ivory Coast (36.1%) [33] (Table 2).…”

Section: Discussionmentioning

confidence: 99%

Genetic Polymorphism of the Glutathione S-Transferase M1 and T1 Genes in Three Distinct Arab Populations

et al. 2011

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“…Genotypes were scored independently by two investigators (KAG and KKB). On the basis of the empiric evidence for associations of this genotype across multiple conditions [17,29-31], individuals were categorized as GSTM1-null (homozygous for deletion) or GSTM1-present (one or two copies of functional allele). Individuals with an absent or faint CYP1a1 band ( n = 8 from VARA and n = 25 from SONORA) were excluded from further analyses, leaving available data from 703 VARA individuals and 610 SONORA participants for analysis.…”

Section: Methodsmentioning

confidence: 99%

Anticitrullinated protein antibody (ACPA) in rheumatoid arthritis: influence of an interaction between HLA-DRB1 shared epitope and a deletion polymorphism in glutathione s-transferasein a cross-sectional study

et al. 2010

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IntroductionA deletion polymorphism in glutathione S-transferase Mu-1 (GSTM1-null) has previously been implicated to play a role in rheumatoid arthritis (RA) risk and progression, although no prior investigations have examined its associations with anticitrullinated protein antibody (ACPA) positivity. The purpose of this study was to examine the associations of GSTM1-null with ACPA positivity in RA and to assess for evidence of interaction between GSTM1 and HLA-DRB1 shared epitope (SE).MethodsAssociations of GSTM1-null with ACPA positivity were examined separately in two RA cohorts, the Veterans Affairs Rheumatoid Arthritis (VARA) registry (n = 703) and the Study of New-Onset RA (SONORA; n = 610). Interactions were examined by calculating an attributable proportion (AP) due to interaction.ResultsA majority of patients in the VARA registry (76%) and SONORA (69%) were positive for ACPA with a similar frequency of GSTM1-null (53% and 52%, respectively) and HLA-DRB1 SE positivity (76% and 71%, respectively). The parameter of patients who had ever smoked was more common in the VARA registry (80%) than in SONORA (65%). GSTM1-null was significantly associated with ACPA positivity in the VARA registry (odds ratio (OR), 1.45; 95% confidence interval (CI), 1.02 to 2.05), but not in SONORA (OR, 1.00; 95% CI, 0.71 to 1.42). There were significant additive interactions between GSTM1 and HLA-DRB1 SE in the VARA registry (AP, 0.49; 95% CI, 0.21 to 0.77; P < 0.001) in ACPA positivity, an interaction replicated in SONORA (AP, 0.38; 95% CI, 0.00 to 0.76; P = 0.050).ConclusionsThis study is the first to show that the GSTM1-null genotype, a common genetic variant, exerts significant additive interaction with HLA-DRB1 SE on the risk of ACPA positivity in RA. Since GSTM1 has known antioxidant functions, these data suggest that oxidative stress may be important in the development of RA-specific autoimmunity in genetically susceptible individuals.

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“…A large proportion of the human population displays a homozygous deletion in the GSTM1 and GSTT1 genes, this null phenotype being associated with malignancies and inflammatory bowel disease. [82] Ollier et al [83] showed an association between the homozygous deletion in the GSTM1 gene and the profile of autoantibodies against ribonuclear proteins (SS-A+/SS-B-) in patients with the inflammatory autoimmune disease and systemic lupus erythematosus (SLE), whilst Morinobu et al [84] found that the frequency of the latter genotype was increased in patients with the autoimmune exocrinopathy, Sjögren's syndrome. Mattey et al [85] recently analyzed the frequency of a number of different GSTT, GSTM and GSTP genotypes in patients with RA compared with healthy controls.…”

Section: Glutathione-s-transferasementioning

confidence: 99%

Advances in Understanding the Genetic Basis of Rheumatoid Arthritis and Osteoarthritis

Chernajovsky

Winyard

Kabouridis

2002

American Journal of PharmacoGenomics

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Rheumatoid arthritis (RA) and osteoarthritis (OA) are polygenic diseases. Polymorphisms in candidate genes have been studied for possible association with susceptibility to disease development. Aside from HLA polymorphisms, of particular interest are those in genes encoding cytokines, signaling molecules, and enzymes involved in the production and catabolism of oxygen and nitrogen radicals. Cytokines are involved in the modulation of the pathological process and have been the target for novel therapeutic interventions. Evidence for their involvement in RA and OA has been provided from genetic analyses in patient populations as well as from animal models of disease. Intracellular signaling cascades control cellular responses and thus regulate many aspects of the pathology manifested in rheumatic diseases. Deciphering the organization and activity of such signaling pathways in disease is underway. Polymorphisms have been identified in gene promoter regions regulating efficient binding of transcription factors, and in coding regions of genes whose products are involved in signal cascades relevant to RA. Among these are the NF-kappaB pathway, steroid receptors and the p53 tumor suppressor gene. Both reactive oxygen species (ROS) and reactive nitrogen species (RNS) have also been implicated in rheumatic diseases. It is thought that excess, damaging, ROS/RNS may arise from an imbalance between the production and removal of these chemical species. Polymorphisms in genes that encode enzymes involved in either generating or degrading ROS/RNS may contribute to such an imbalance. In the last few years, polymorphisms in such genes have indeed been identified as risk factors for rheumatic diseases.

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Association of the glutathione S-transferase M1 homozygous null genotype with susceptibility to Sj�gren's syndrome in Japanese individuals

Abstract: The GSTM1 homozygous null genotype could be a genetic factor that determines susceptibility to SS and may be involved in SSA antibody production.

Cited by 36 publications

References 14 publications

Genetic Polymorphism of the Glutathione S-Transferase M1 and T1 Genes in Three Distinct Arab Populations

Genetic Polymorphism of the Glutathione S-Transferase M1 and T1 Genes in Three Distinct Arab Populations

Anticitrullinated protein antibody (ACPA) in rheumatoid arthritis: influence of an interaction between HLA-DRB1 shared epitope and a deletion polymorphism in glutathione s-transferasein a cross-sectional study

Advances in Understanding the Genetic Basis of Rheumatoid Arthritis and Osteoarthritis

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