Regulation of TREG functionality by acetylation-mediated FOXP3 protein stabilization. FOXP3 interactions with histone acetyltransferase and class II histone deacetylases are required for repression. Histone deacetylase 6 and heat shock protein 90 control the functions of FOXP3 + T-regulatory cells. Inhibition of HDAC9 increases T regulatory cell function and prevents colitis in mice. Histone deacetylases 6 and 9 and sirtuin-1 control FOXP3 + regulatory T cell function through shared and isoform-specific mechanisms. Function of histone deacetylase inhibitors in inflammation. Increased activity and expression of histone deacetylase 1 in relation to tumor necrosis factor-α in synovial tissue of rheumatoid arthritis. Histone deacetylase/acetylase activity in total synovial tissue derived from rheumatoid arthritis and osteoarthritis patients. Expression and function of histone deacetylases in rheumatoid arthritis synovial fibroblasts. Operating on chromatin, a colorful language where context matters.
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What do microRNAs mean for rheumatoid arthritis? Arthritis Rheum. DNA methylome signature in rheumatoid arthritis. DNA methylation regulates the expression of CXCL12 in rheumatoid arthritis synovial fibroblasts. Functions of DNA methylation: islands, start sites, gene bodies and beyond. Inflammatory memories: is epigenetics the missing link to persistent stromal cell activation in rheumatoid arthritis? Autoimmun. Duality of fibroblast-like synoviocytes in RA: passive responders and imprinted aggressors. (Eds) Epigenetic Mechanisms of Gene Regulation (Cold Spring Harbor Laboratory Press, Woodbury, 1996).īottini, N. The molecular and mathematical basis of Waddington's epigenetic landscape: a framework for post-Darwinian biology? Bioessays 34, 149–157 (2012). Epigenetic alterations in autoimmune rheumatic diseases. Genetic predisposition of the severity of joint destruction in rheumatoid arthritis: a population-based study. Genetics of rheumatoid arthritis: what have we learned? Immunogenetics 63, 459–466 (2011). Twin studies in autoimmune disease: genetics, gender and environment.
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Such an approach could also facilitate the development of strategies to target these epigenetic modifications in the clinic.īogdanos, D. Herein, we highlight studies, the findings of which collectively suggest that revisiting the original definition of epigenetics, conceived some 70 years ago, might advance our interpretation of DNA and histone modifications with regard to gene expression and clinical outcome in RA. A surprising theme emerging from studies of the enzymes responsible for these epigenetic modifications, particularly histone deacetylases, is that they regulate inflammatory activation of cell populations relevant to RA through independent, direct, and dynamic interactions with nonhistone proteins. Efforts to understand the nongenetic contributions to RA disease susceptibility have recently focused on the study of epigenetic mechanisms, namely modifications of DNA and histones, which are subject to environmental influences and regulate gene expression. Genome-wide association studies have shown that genetic polymorphisms make a substantial but incomplete contribution to the risk of developing rheumatoid arthritis (RA).