Transforming growth factor beta1 gene polymorphism in rheumatoid arthritis

Sugiura, Yoshiki; Niimi, Takashi; Sato, Shigeki; Yoshinouchi, Takeo; Banno, Shogo; Naniwa, Taio; Maeda, Hanako; Shimizu, Shuhei; Ueda, Ryuzo

doi:10.1136/ard.61.9.826

Cited by 72 publications

(46 citation statements)

References 15 publications

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“…22 Different genetic backgrounds between whites and Japanese may explain, at least in part, the disparate findings of the studies. The possible existence of ethnicity-specific association profiles may be reflected by the significantly different allele frequencies and genotype distributions of the 868T/C SNP between the present white population and populations from Japan, including the sample examined by Yokota et al 20,22,37 Heterogeneities in the prevalences of conventional risk factors for MI, including arterial hypertension, hypercholesterolemia, cigarette smoking, and diabetes mellitus, may have contributed also to the divergent results between the study populations.…”

Section: Discussionmentioning

confidence: 81%

Association of Transforming Growth Factor-β1 Gene Polymorphisms With Myocardial Infarction in Patients With Angiographically Proven Coronary Heart Disease

Koch

Hoppmann

Mueller

et al. 2006

ATVB

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Objective-Transforming growth factor (TGF)-␤1 (TGF-␤1) is a multifunctional cytokine that exhibits vasculoprotective properties. Production and plasma levels of TGF-␤1 are influenced by polymorphisms in the TGF-␤1 gene (TGFB1). We investigated whether the Ϫ509C/T (rs1800469), 868T/C (rs1982073), 913G/C (rs1800471), and 11929C/T (rs1800472) polymorphisms of TGFB1 are associated with myocardial infarction. Methods and Results-The study population consisted of 3657 patients with myocardial infarction (885 women and 2772 men) and 1211 control individuals (598 women and 613 men) with angiographically normal coronary arteries and without signs or symptoms of myocardial infarction. Polymorphism-related genotypes were determined with TaqMan assays and haplotypes were estimated from the genotype data. The Ϫ509C/T polymorphism and Ϫ509C/868T/913G/ 11929C (CTGC) haplotype were associated with myocardial infarction in men, independently from the potentially confounding factors age, arterial hypertension, hypercholesterolemia, cigarette smoking, and diabetes mellitus.

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Section: Discussionmentioning

confidence: 81%

Association of Transforming Growth Factor-β1 Gene Polymorphisms With Myocardial Infarction in Patients With Angiographically Proven Coronary Heart Disease

Koch

Hoppmann

Mueller

et al. 2006

ATVB

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“…The characteristic in the joint is the excessive proliferation of synovial cells, antigen-presenting cells, and infiltrating leukocytes, where both T and B cells mediate the inflammatory network that contributing to the joint damage [4,5]. There is evidence of genetic factors in RA, including several cytokine genes, which have been considered as possible candidates to influence the susceptibility of the disease [6].…”

Section: Introductionmentioning

confidence: 98%

The functional class evaluated in rheumatoid arthritis is associated with soluble TGF-β1 serum levels but not with G915C (Arg25Pro) TGF-β1 polymorphism

et al. 2010

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The influence of genetic factors in rheumatoid arthritis (RA) has been described, including several cytokine genes such as transforming growth factor β (TGF-β) with regulatory effects on lymphocytes, dendritic cells, macrophages, chondrocytes, and osteoblasts, which are important in the RA pathogenesis. The G915C TGF-β1 polymorphism has been associated with soluble TGF-β1 (sTGF-β) serum levels. Thus, we studied the association of G915C (Arg25Pro) TGF-β1 polymorphism with sTGF-β1 serum levels in RA. We enrolled 120 RA patients and 120 control subjects (CS). The G915C TGF-β1 polymorphism was determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method, and sTGF-β1 serum levels were quantified using an ELISA kit. The genotype frequency of G915C TGF-β1 polymorphism in RA and CS was G/G (91.7%), G/C (8.3%), C/C (0%) and G/G (85.8%), G/C (14.2%), C/C (0%), respectively, without significant differences. Moreover, the G/G TGF-β1 genotype carriers presented the highest disability index evaluated for the Spanish HAQ-DI score (P < 0.001). In addition, the sTGF-β1 serum levels were higher in RA (182.2 ng/mL) than CS (160.2 ng/mL), there was not significant difference. However, we found a positive correlation between the sTGF-β1 serum levels and the functional class (r = 0.472, P = 0.023). In conclusion, the G915C (Arg25Pro) TGF-β1 polymorphism is not associated with RA, but the sTGF-β1 serum levels are related with the functional class in RA.

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“…Genetic polymorphisms in the TGF-β gene have been shown to interfere with the production, secretion or activity of this growth factor (Atilla et al 2006;Awad et al 1998;Li et al 1999) and this has been associated with risk for systemic diseases including cardiovascular diseases and rheumatoid arthritis, which are related to periodontitis in terms of chronic inflammatory processes (Atilla et al 2006;Garcia Henshaw and Krall 2001;Mercado Marshall and Bartold 2003;Sugiura et al 2002). Epithelial surfaces up-regulate TGF-β in response to infection with other non-oral bacterial pathogens, including Yersinia, Cryptosporidium, EHEC O157:H7 and EPEC (Howe et al 2005).…”

Section: Tgf-β Signaling Pathwaymentioning

confidence: 99%

Beyond Good and Evil in the Oral Cavity: Insights into Host-Microbe Relationships Derived from Transcriptional Profiling of Gingival Cells

2008

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In many instances, the encounter between host and microbial cells can be, through a longstanding evolutionary association, a balanced interaction whereby both cell types co-exist and inflict a minimal degree of harm on each other. In the oral cavity, despite the presence of large numbers of diverse organisms, health is the most frequent status. Disease will only ensue when the host-microbe balance is disrupted on a cellular and molecular level. With the advent of microarrays, it is now possible to monitor the responses of host cells to bacterial challenge in a global scale. However, microarray data are known to be inherently noisy, which is caused in part by their great sensitivity. Hence, we will address a number of important general considerations required to maximize the significance of microarray analysis in order to faithfully depict relevant host-microbe interactions. Several advantages and limitations of microarray analysis that may directly impact the significance of array data are highlighted and discussed. Further, this review revisits and contextualizes recent transcriptional profiles that were originally generated to specifically study intricate cellular interactions between gingival cells and four important plaque microorganisms. This is, to our knowledge, the first report that systematically investigates the cellular responses of a cell line to challenge by 4 different microorganisms. Of particular relevance to the oral cavity, the model bacteria span the entire spectrum of documented pathogenic potential from commensal to opportunistic to overtly pathogenic. These studies provide a molecular basis of the complex and dynamic interaction between the oral microflora and its host, which may lead, in the long run, to the development of novel, rational and practical therapeutic, prophylactic and diagnostic applications.

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Transforming growth factor beta1 gene polymorphism in rheumatoid arthritis

Cited by 72 publications

References 15 publications

Association of Transforming Growth Factor-β1 Gene Polymorphisms With Myocardial Infarction in Patients With Angiographically Proven Coronary Heart Disease

Association of Transforming Growth Factor-β1 Gene Polymorphisms With Myocardial Infarction in Patients With Angiographically Proven Coronary Heart Disease

The functional class evaluated in rheumatoid arthritis is associated with soluble TGF-β1 serum levels but not with G915C (Arg25Pro) TGF-β1 polymorphism

Beyond Good and Evil in the Oral Cavity: Insights into Host-Microbe Relationships Derived from Transcriptional Profiling of Gingival Cells

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