The C-509T and T869C functional polymorphisms of TGF-beta(1) gene do not represent a genetic predisposition to COPD susceptibility in Hong Kong Chinese patients.
The fibroblasts that resist CSE-induced cellular senescence may contribute to the pathogenesis of idiopathic pulmonary fibrosis and could contribute to fibrotic lesions in chronic obstructive pulmonary disease acting through a TGF-β1-mediated pathway.
The FPRP test results were as follows: 1) when the prior probability was 0.001 and the OR was 1.5, ADAM33 rs612709, CHRNA3/5 rs1051730, CHRNA3/5 rs8034191, CHRNA3/5 rs16969968, and TGFB1rs1800470 were truly associated with COPD risk (FPRP < 0.2); 2) when the prior probability was 0.000001 and the OR was 1.5, all the variants except TGFB1rs1800470 remained noteworthy; and 3) when the probability was 0.000001 and the OR was 1.2, ADAM33 rs612709 and CHRNA3/5 rs1051730 remained true positives.
The gene expression profile indicated altered activity of upstream mediators associated with COPD pathophysiology, including hepatocyte growth factor, transforming growth factor beta 1 and platelet-derived growth factor B, which suggests that COPD-related changes in the bronchial ECM contribute to the defective regenerative ability in the airways of COPD patients.
The levels of IL-1β, TNF-α, p-NF-κB, p-IκBα, TGF-β1 and Smad2 were significantly higher in COPD rats than in controls, while they were dramatically reduced in the three TCM- and aminophylline-treated groups.
The plasma concentrations of IL-6, TGF-β1 and IL-12 were significantly increased in patients with COPD compared with never-smokers and smokers with normal lung function.
The polymorphism 869T/C in TGF-beta1 gene has a significant association with disease occurrence in COPD patients and the C allele might be a risk factor.
The single nucleotide polymorphism (SNP) in the TGF-beta1 gene promoter might be associated with COPD, and the -800A/-509C haplotype is possibly one of the susceptibility factors for COPD.
The test-replication approach identified four genes-microsomal epoxide hydrolase (EPHX1), latent transforming growth factor-beta binding protein-4 (LTBP4), surfactant protein B (SFTPB), and transforming growth factor-beta1 (TGFB1)-that were associated with COPD-related phenotypes.
This study compared the expression of PI3K isoforms by ASM cells from donors with asthma (A), chronic obstructive pulmonary disease (COPD), or neither disease (NA), and investigated the role of PI3K isoforms in the production of TGFβ1 induced pro-inflammatory cytokine and contractile proteins in ASM cells.
Two SNPs in TGFB1 (C to T substitution at nucleotide -509 and substitution of leucine 10 with proline (Leu10Pro)), Leu50Val in SFTPA1 and Ala160Thr in SFTPD showed evidence suggestive of association with FEV(1)/IVC in subjects with GOLD stage >or=2 COPD.
VEGF mRNA levels were 18% higher in COPD patients compared with controls (p = 0.04), while for the obese patients, these levels were not statistically significantly different. bFGF and TGF-beta(1) mRNA levels in COPD patients or obese individuals compared with controls did not differ significantly either.
We designed this study to evaluate relation between Transforming Growth Factor Beta1 (TGFß1) and Tissue Inhibitory of Metaloproteinase 2 (TIMP2) as two main tissue mediators on activity and reversibility of asthma and chronic obstructive pulmonary disease (COPD).
With respect to T869C polymorphism, a significant association of TGF-β 1 gene polymorphism at 869T/C with COPD was observed in the overall analysis (C vs. T: OR 0.82, 95%CI 0.70-0.96, P = 0.01).
[Expression of secretory leukocyte proteinase inhibitor in the bronchi and lung tissues of chronic obstructive pulmonary disease rat models and the regulatory mechanism by transforming growth factor beta(1)].