These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Promoter Hypermethylation of GATA3, IL-4, and TGF-β Confers Susceptibility to Vogt-Koyanagi-Harada Disease in Han Chinese. Author: Zhu Y, Yu H, Qiu Y, Ye Z, Su W, Deng J, Cao Q, Yuan G, Kijlstra A, Yang P. Journal: Invest Ophthalmol Vis Sci; 2017 Mar 01; 58(3):1529-1536. PubMed ID: 28278322. Abstract: PURPOSE: We investigated the role of promoter methylation of transcriptional and inflammatory factors, including TBX21, GATA3, RORγt, FOXP3, IFN-γ, IL-4, IL-17A, and TGF-β in the development of Vogt-Koyanagi-Harada (VKH) disease. METHODS: The promoter methylation levels were detected by the Sequenom MassARRAY system in CD4+ T cells that were separated from 20 healthy individuals and 32 VKH patients (20 in the active stage without medication, 12 in inactive stage with medication). The mRNA expression level of GATA3, IL-4, and TGF-β in CD4+ T cells was analyzed by real-time RT-PCR. RESULTS: The promoter methylation levels of GATA3, IL-4, and TGF-β were significantly higher in active VKH patients than in healthy individuals (P < 0.05). A decreased mRNA expression of GATA3 and TGF-β was found in active VKH patients, which was correlated negatively with the DNA methylation of these factors. Treatment with systemic corticosteroid and cyclosporin A (CsA) decreased the methylation level of GATA3 and TGF-β in association with an increased mRNA expression of molecules and reduced disease activity. CONCLUSIONS: Our findings suggest that promoter hypermethylation of GATA3 and TGF-β in CD4+ T cells confers risk to VKH disease in Han Chinese.[Abstract] [Full Text] [Related] [New Search]