AIM: Tumor necrosis factor α (TNF-α) influences the pathogenesis of lung-fibrosis and carcinogenesis in normal cells. Polymorphisms of this gene are suggested to be associated with susceptibility to lung-diseases. Additionally TNF-α is postulated to play a significant role in regulating. Transforming growth factor (TGF-β₁) expression Therefore we investigated if the TNF-α or TGF-β₁ gene expression level is different within the -308 TNF-α genotypes. METHODS: Quantitative Real-time PCR of TNF-α and TGF-β₁ was performed in 178 Germans. Calculations of expression were made with the 2(-ΔΔCT) method. Detection of the -308 promoter polymorphism of the TNF-α gene was performed by rapid capillary PCR with melting curve analysis. RESULTS: The relative TNF-α mRNA expression revealed significant differences between the TNF-α -308 homozygote wild-type G/G (0.00079±0.00011; n=113) and the heterozygote genotype G/A (0.0005±0.00008; n=52; p=0.030) as well as between homozygote wild-type G/G and the homozygote mutant A/A (0.00029±0.00009; n=5; p=0.004). The relative TGF-β mRNA expression showed, similar to TNF-α, the highest mRNA expression was seen within the TNF-α -308 homozygote wild-types, while the lowest mRNA expression lay within the homozygote mutant-types. CONCLUSION: Our findings suggest that the G-allele of TNF-α -308 is associated with a significantly higher TNF-α mRNA expression compared to the A-allele and that this also reflects in TGF-β expression. Therefore we support the thesis that TGF-β is regulated by TNF-α.
AIM: Tumor necrosis factor α (TNF-α) influences the pathogenesis of lung-fibrosis and carcinogenesis in normal cells. Polymorphisms of this gene are suggested to be associated with susceptibility to lung-diseases. Additionally TNF-α is postulated to play a significant role in regulating. Transforming growth factor (TGF-β₁) expression Therefore we investigated if the TNF-α or TGF-β₁ gene expression level is different within the -308 TNF-α genotypes. METHODS: Quantitative Real-time PCR of TNF-α and TGF-β₁ was performed in 178 Germans. Calculations of expression were made with the 2(-ΔΔCT) method. Detection of the -308 promoter polymorphism of the TNF-α gene was performed by rapid capillary PCR with melting curve analysis. RESULTS: The relative TNF-α mRNA expression revealed significant differences between the TNF-α -308 homozygote wild-type G/G (0.00079±0.00011; n=113) and the heterozygote genotype G/A (0.0005±0.00008; n=52; p=0.030) as well as between homozygote wild-type G/G and the homozygote mutant A/A (0.00029±0.00009; n=5; p=0.004). The relative TGF-β mRNA expression showed, similar to TNF-α, the highest mRNA expression was seen within the TNF-α -308 homozygote wild-types, while the lowest mRNA expression lay within the homozygote mutant-types. CONCLUSION: Our findings suggest that the G-allele of TNF-α -308 is associated with a significantly higher TNF-α mRNA expression compared to the A-allele and that this also reflects in TGF-β expression. Therefore we support the thesis that TGF-β is regulated by TNF-α.
Authors: Julienne E Bower; Patricia A Ganz; Michael R Irwin; Steven Castellon; Jesusa Arevalo; Steven W Cole Journal: J Clin Oncol Date: 2013-03-25 Impact factor: 44.544
Authors: José Francisco Muñoz-Valle; Edith Oregón-Romero; Héctor Rangel-Villalobos; Gloria Esther Martínez-Bonilla; Eduardo Castañeda-Saucedo; Lorenzo Salgado-Goytia; Marco Antonio Leyva-Vázquez; Berenice Illades-Aguiar; Luz del Carmen Alarcón-Romero; Mónica Espinoza-Rojo; Isela Parra-Rojas Journal: Clin Exp Med Date: 2012-10-30 Impact factor: 3.984
Authors: Erik J M Toonen; Pilar Barrera; Jaap Fransen; Arjan P M de Brouwer; Agnes M Eijsbouts; Pierre Miossec; Hubert Marotte; Hans Scheffer; Piet L C M van Riel; Barbara Franke; Marieke J H Coenen Journal: Arthritis Res Ther Date: 2012-12-07 Impact factor: 5.156