The 2.5 kb TGF-beta 1 mRNA was seen in all 18 samples analysed by Northern blotting and densitometric analysis showed no difference between the asthmatic group (mean (SD) 108% (43%)), the group with COPD (122% (33%)), and the non-obstructed group (100% (49%)).
Spontaneously released immunoreactive TGF-beta1 levels from cultured epithelial cells were more elevated in subjects with a history of smoking and patients with COPD than in nonsmokers.
Transforming growth factor-beta1 is a potent mediator of fibrosis stimulating the secretion of extracellular matrix proteins and is involved in airway remodeling in chronic obstructive pulmonary disease (COPD).
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.
Abnormal expression of TGF-beta1 is believed to play an important role in the pathogenesis of a number of chronic inflammatory and immune lung diseases, including asthma, chronic obstructive pulmonary disease, and pulmonary fibrosis.
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.
[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)].
Eight SNPs in TGFB1 (rs2241712, rs1982072, and rs1800469 in the promoter region; rs1982073 in exon 1; rs2241716 and rs4803455 in intron 2; rs6957 and rs2241718 in the 3' region) were genotyped by allelic discrimination assays in 70 COPD patients with emphysema phenotype and 99 healthy smokers.
Published human microarray and murine linkage studies have also demonstrated the importance of TGFBR3 in emphysema and lung function, and our group and others have previously found association of COPD-related traits with TGFB1, a ligand for TGFBR3.
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.
In addition, increased expression of TGF-beta1 in COPD lungs and primary cells, such as epithelial cells, macrophages, or fibroblasts isolated from COPD specimens, was reported, suggesting an impact of TGF-beta signalling on the development and progression of COPD.
Of these variants, four were significantly associated with COPD susceptibility in random effects meta-analysis, the GSTM1 null variant (OR 1.45, CI 1.09-1.92), rs1800470 in TGFB1 (0.73, CI 0.64-0.83), rs1800629 in TNF (OR 1.19, CI 1.01-1.40) and rs1799896 in SOD3 (OR 1.97, CI 1.24-3.13).
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.
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).
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.
LPS directly induced CTGF expression in bronchial epithelial cells, independently of transforming growth factor-beta1, suggesting a possible mechanism for airway remodelling in COPD that is induced by smoking and repeated bacterial infections.
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).