Tumor necrosis factor-alpha inhibitors suppress CCL2 chemokine in monocytes via epigenetic modification - Lin, Yi-Ching; Lin, Yu-Chih; Huang, Ming-Yii; Kuo, Po-Lin; Wu, Cheng-Chin; Lee, Min-Sheng; Hsieh, Chong-Chao; Kuo, Hsuan-Fu; Kuo, Chang-Hung; Tsai, Wen-Chan; Hung, Chih-Hsing (Molecular immunology, 2017)
Keywords: acetylation; acetyltransferases; Adalimumab - pharmacology; adverse effects; Arthritis, Rheumatoid - genetics; Arthritis, Rheumatoid - immunology; Blotting, Western; CCL2; chemokine CCL2; Chemokine CCL2 - biosynthesis; Chemokine CCL2 - genetics; chromatin; Chromatin Immunoprecipitation; DNA Methylation; enzyme-linked immunosorbent assay; Epigenesis, Genetic; Epigenetic regulation; epigenetics; Etanercept - pharmacology; gene expression; gene expression regulation; Gene Expression Regulation - drug effects; histones; Histones - genetics; Histones - metabolism; Humans; immunomodulation; methyltransferases; mitogen-activated protein kinase; Monocyte; monocytes; Monocytes - drug effects; Monocytes - immunology; Monocytes - metabolism; pathogenesis; precipitin tests; promoter regions; Promoter Regions, Genetic - genetics; Rheumatoid arthritis; TNF-α inhibitors; transcription factor NF-kappa B; tumor necrosis factor-alpha; Tumor Necrosis Factor-alpha - antagonists & inhibitors; Western blotting; MCP-1; pp65; Epigenetic regulation; ChIP; LPS; H3K36me3; Cmin; CBP; pp38; NF-κB; CCL2; Cmax; IL; pJNK; Monocyte; H3K4me3; H3K79me3; H3; MAPK; RA; TNF-α; Rheumatoid arthritis; HAT; SEM; pERK; PCAF; HDAC; ELISA; H3K27me3; TNF-α inhibitors