Relationship between TGF-β1 + 869 T/C and + 915 G/C gene polymorphism and risk of acute rejection in renal transplantation recipients

Li, Hongyan; Zhou, Tian-Biao; Lin, Shujun; Lin, Wen‐Shan

doi:10.1186/s12881-019-0847-2

Cited by 6 publications

(5 citation statements)

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“…Di et al (2017) also found the SNP rs1800468 locus and the signal peptide rs1800471 locus also located in the promoter region are correlated with the expression level of TGF-b1 in plasma, and that specific alleles of these poly-morphisms were closely related to lung cancer susceptibility. Li et al (2019) also showed that the SNP located at the rs1800470 of the signal peptide of TGF-b1 gene is closely related to the occurrence of chronic obstructive pulmonary disease.…”

Section: Introductionmentioning

confidence: 95%

Association of Transforming Growth Factor β1 Gene Polymorphisms and Inflammatory Factor Levels with Susceptibility to Sepsis

Zheng¹,

Fu²,

Zhao

2021

Genetic Testing and Molecular Biomarkers

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To study the association of transforming growth factor b1 (TGF-b1) gene single nucleotide polymorphisms (SNPs) and plasma TGF-b1 levels with susceptibility to sepsis. Methods: The genotypes of the TGF-b1 gene rs1800469, rs1800468, rs1800470, and rs1800471 loci in 285 sepsis patients (119 patients with severe sepsis and 166 patients with mild sepsis) and 285 healthy individuals (control group) were analyzed through Sanger sequencing. Enzyme-linked immunosorbent assay was used to detect the levels of plasma inflammatory factors. Results: The TGF-b1 gene SNP rs1800469 C allele was 0.56 times lower than the T allele in terms of risk of susceptibility to sepsis (95% confidence interval [CI]: 0.43-0.72, p < 0.01). Carriers of the A allele at the rs1800468 locus of the TGF-b1 were 2.82 times more susceptible to sepsis than those with the G allele (95% CI: 1.62-4.91, p < 0.01). The T allele at the rs1800470 locus of TGF-b1 produced a lower risk of sepsis than those with the C allele (odds ratio [OR] = 0.74, 95% CI: 0.57-0.94, p = 0.02). The risk of susceptibility to sepsis in the TGF-b1 rs1800471 locus G allele was 3.54 times higher than that of C allele (95% CI: 2.14-5.86, p < 0.01). The TGF-b1 gene rs1800469 T > C and rs1800470 C > T were associated with mild sepsis, whereas rs1800468 G > A and rs1800471 C > G were associated with severe sepsis ( p < 0.01). The TGF-b1 gene rs1800469 T > C and rs1800470 C > T were associated with lower plasma TGF-b1 levels, whereas rs1800468 G > A and rs1800471 C > G were associated with higher TGF-b1 levels ( p < 0.05). Conclusion:The alleles T > C of rs1800469 and C > T of rs1800470 of the TGF-b1 gene were associated with lower plasma TGF-b1 levels and a reduced risk of sepsis susceptibility, whereas the alleles rs1800468 G > A and rs1800471 C > G were associated with higher TGF-b1 levels and risk of susceptibility to sepsis.

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Section: Introductionmentioning

confidence: 95%

Association of Transforming Growth Factor β1 Gene Polymorphisms and Inflammatory Factor Levels with Susceptibility to Sepsis

Zheng¹,

Fu²,

Zhao

2021

Genetic Testing and Molecular Biomarkers

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“…Результаты и выводы различных исследований генетического полиморфизма TGFB1 у реципиентов солидных органов не всегда однозначны, что может быть связано с недостаточным количеством изучаемых случаев, этнической неоднородностью выборки, а также с различиями в определении исследуемых фенотипов и применением различных методов анализа. Для обобщения разнородных исследований часто используют метаанализ и систематические обзоры, которые проводятся в соответствии с определенными стандартами и позволяют, как полагают, привести к общему знаменателю разобщенные данные [18,28,43].…”

Section: Abstract: Single-nucleotide Polymorphism Graft Rejection Graft Fibrosis Graft Dysfunctionunclassified

“…Например, метаанализ 18 исследований, посвященных поиску связи полиморфизма в гене цитокина TGF-β1 в позициях +869T/C и +915G/C с развитием острого отторжения у реципиентов почки, показал, что эти факторы не связаны между собой [28].…”

Section: Abstract: Single-nucleotide Polymorphism Graft Rejection Graft Fibrosis Graft Dysfunctionunclassified

“…Исследования генетического полиморфизма гена TGFB1 при трансплантации солидных органов проведены главным образом у реципиентов почки и печени [25][26][27][28] и значительно меньше -у реципиентов сердца, что обусловлено числом проводимых трансплантаций сердца [29][30][31]. Как правило, исследуемые исходы включали острое и хроническое отторжение, среднесрочную функцию трансплантата, концентрации такролимуса, впервые возникший диабет после трансплантации, развитие фиброза трансплантата, а также частоту инфекционных заболеваний.…”

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The role of TGF-β1 gene polymorphisms in the development of post-transplant complications

Курабекова

Гичкун

Мещеряков

et al. 2021

RJTAO

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Transforming growth factor beta 1 (TGF-β1) is an immunosuppressive and profibrogenic cytokine capable of influencing the development of graft rejection and graft fibrosis in solid organ recipients. The TGF-β gene has a significant polymorphism that may cause individual protein expression levels and be associated with post-organ transplant complications. It is believed that three TGFB1 polymorphic variants (rs1800469, rs1800470 and rs1800471) may be associated with the development of graft rejection, graft fibrosis and chronic dysfunction of a heart, liver or kidney transplant. A review of current literature presents the results of studies on the relationship between TGF-β1 gene polymorphisms and post-transplant complications in solid organ recipients. The findings of various studies of TGF-β1 gene polymorphism in solid organ recipients are not always unambiguous, and their results are often difficult to generalize even with the help of meta-analysis. Samples included in studies vary in terms of ethnicity, gender, age, and underlying medical conditions, while results are highly dependent on sample structure or latent relatedness. Currently available data suggest that TGFB1 polymorphism may determine a predisposition to the development of graft rejection, graft fibrosis and graft dysfunction in solid organ recipients, but this is not conclusive and requires further, larger studies.

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“…Although Gαs-mediated signaling participates in a number of pathophysiological processes by initiating diverse intracellular signaling cascades, until now no studies have elucidated the role of the functional GNAS c.393C>T polymorphism in the clinical outcome of renal transplant recipients. However, increasing evidence suggests that inherited factors may affect renal allograft survival [ 18 , 19 , 20 , 21 ]. Regarding the relationship with the renal allograft outcome, G-protein-mediated receptor signaling is a promising candidate because it is a part of angiotensin II, chemokine, and adrenergic receptor signaling, which is involved in the immunological processes of the formation of donor-specific antibodies (DSAs) and the development of rejections [ 4 , 22 , 23 ].…”

Section: Introductionmentioning

confidence: 99%

CC Genotype of GNAS c.393C>T (rs7121) Polymorphism Has a Protective Effect against Development of BK Viremia and BKV-Associated Nephropathy after Renal Transplant

et al. 2022

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The GNAS gene encodes the alpha-subunit of the stimulatory G-protein (Gαs) in humans and mice. The single-nucleotide polymorphism of GNAS, c.393C>T, is associated with an elevated production of Gαs and an increased formation of cyclic adenosine monophosphate (cAMP). In the present study, we analyzed the effect of this GNAS polymorphism on a renal allograft outcome. We screened a cohort of 436 renal allograft recipients, who were retrospectively followed up for up to 5 years after transplant. GNAS genotypes were determined with polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) assays. The 393T allele was detected in 319 (73%) recipients (113 recipients with TT and 206 with CT genotype) and the CC genotype in 117 (27%). The CC genotype was associated with a significantly lower frequency of BK viremia (CC, 17 recipients (15%); T 84 (26%)); p = 0.01; TT, 27 vs. CC, 17, p = 0.07; TT, 27 vs. CT, 57, p = 0. 46; CT, 57 vs. CC, 17, p = 0.01) and BKV-associated nephropathy (CC, 3 recipients (3%); T, 27 (8%); p = 0.03; TT,10 vs. CC, 3, p = 0.04; TT, 10 vs. CT,17, p = 0.85; CT, 17 vs. CC,3, p = 0.04) after transplant. BKV-associated nephropathy-free survival was significantly better among CC genotype carriers than among T allele carriers (p = 0.043; TT vs. CC, p = 0.03; CT vs. CC, p = 0.04; TT vs. CT, p = 0.83). Multivariate analysis indicated an independent protective effect of the CC genotype against the development of both BK viremia (relative risk. 0.54; p = 0.04) and BKV-associated nephropathy after renal transplant (relative risk. 0.27; p = 0.036). The GNAS 393 CC genotype seems to protect renal allograft recipients against the development of BK viremia and BKV-associated nephropathy.

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Relationship between TGF-β1 + 869 T/C and + 915 G/C gene polymorphism and risk of acute rejection in renal transplantation recipients

Cited by 6 publications

References 54 publications

Association of Transforming Growth Factor β1 Gene Polymorphisms and Inflammatory Factor Levels with Susceptibility to Sepsis

Association of Transforming Growth Factor β1 Gene Polymorphisms and Inflammatory Factor Levels with Susceptibility to Sepsis

The role of TGF-β1 gene polymorphisms in the development of post-transplant complications

CC Genotype of GNAS c.393C>T (rs7121) Polymorphism Has a Protective Effect against Development of BK Viremia and BKV-Associated Nephropathy after Renal Transplant

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