The comparison of serum TGF-beta levels and associated polymorphisms in patients with coronary artery ectasia and normal coronary artery

Abstract

Background Coronary artery ectasia (CAE) is described as the enlargement of a coronary artery segment by 1.5 times or more, which is generally associated with the atherosclerotic process. Atherosclerotic changes lead to arterial remodeling result in CAE. In our study, we measured serum transforming growth factor (TGF)-β1 levels, which have a protective role against atherosclerosis. Further, we aimed to assess the TGF-β1 gene variants rs1800469 (–509C>T, c.−1347C>T) and rs1800470 (c.+29T>C, p.Pro10Leu, rs1982073), which might have an effect on TGF production. Overall, 2877 patients were screened including 56 patients with CAE and 44 patients with normal coronary arteries who were included in the study. Serum TGF-β1 levels were measured using ELISA and compared between two groups. Additionally, TGF-β1 rs1800469 and rs1800470 gene variations were determined using TaqMan® SNP Genotyping Assays. Results Serum TGF-β1 levels were significantly lower in patients with CAE than in controls (p=0.012). However, there was no difference in terms of the genotype and allele distributions of TGF-β1 rs1800469 and rs1800470 polymorphisms. Serum TGF-β1 levels were higher in individuals carrying the TGF-β1 rs1800470 G allele (GG+AG) than in individuals with normal homozygous AA genotype in the CAE group (p=0.012). Conclusion Our findings suggest that lower serum TGF-β1 levels are associated with an increased risk for CAE development and that TGF-β1 polymorphisms exert a protective effect. Furthermore, TGF-β1 rs1800470 G allele carriers were shown to have higher TGF-β1 levels in the CAE group. This suggests that having the G allele in the TGF-β1 rs1800470 polymorphism could prevent CAE development.

Transforming growth factor serum concentrations in patients with proven non-syndromic aortopathy

“…Similar concentrations in DAA and NDAA patients can be attributed to the aortic valve and ascending aorta developing from neural crest cells during embryonic development ( 31 – 34 ). TGF-β1 levels were lower in the coronary artery ectasia group than in the control group, according to Ser et al ( 35 ). This information provided us with additional information indicating possible similarities in the ascending aorta’s anatomical structures.…”

“…When patients were divided into groups based on aortic valve phenotype, there was no statistically significant difference in TGF-β1 levels between DAA-TAV and DAA-BAV [30.39 (24.1-37.44) vs. 37. 35 TGF-β1 concentrations in patients with dilated and non-dilated aortas according to aortic valve cuspidity. CG, control group; DAA-TAV, dilated ascending aorta-tricuspid aortic valve; DAA-BAV, dilated ascending aorta-bicuspid aortic valve; NDAA-TAV, non-dilated ascending aorta-tricuspid aortic valve; NDAA-BAV, non-dilated ascending aorta-bicuspid aortic valve.…”

Decreased circulating transforming growth factor-beta (TGF-β) and kidney TGF-β immunoreactivity predict renal disease in cats with naturally occurring chronic kidney disease

“…A study reported low serum TGF-β concentration in cats with CKD compared with healthy cats, but the findings were not significant. 18 Regarding other diseases, serum TGF-β1 concentration was significantly lower in human patients with thrombocytopenia 31 and coronary artery disease 32,33 than in controls. TGF-β1 is produced by megakaryocytes, stored in platelet alpha-granules and released in serum by degranulation.…”

Tolerogenic dendritic cells generated in vitro using a novel protocol mimicking mucosal tolerance mechanisms represent a potential therapeutic cell platform for induction of immune tolerance

“…Even though AhR agonists, TGF-β, and RA are naturally present at mucosal sites and contributes to tolerance induction, injecting the combination of IGN-512, TGF-b, and RA systemically is not considered a viable option because of the risk of toxicity as the concentrations used for the generation of ItolDCs are higher than what if found in normal serum levels ( 61 , 62 ). Further, it will be very difficult to accomplish antigen-specific tolerance following systemic injection of the antigen, unless the compounds are encapsulated ( 63 ), e.g.…”