Transcriptional responses to TNF following HFl treatment of primary rheumatoid arthritis fibroblast like synoviocytes (RA-FLS)

We report the effects of Hfol on TNF induction of inflammatory genes in wild type cells versus cells depleted of GCN2 RNA-seq analysis of primary rheumatoid arthritis fibroblast like synoviocytes (RA-FLS) treated with TNFa in the presence or absence of Halofuginone (HF). To test the effect of the aminoacyl tRNA synthetase (AARS) inhibitor HF on inflammatory responses in RA-FLS, cells in culture were treated, using duplicate samples for each condition, for 16 hours with HF and 8 or 24 hours with TNFa.

本研究报道了哈夫格鲁宁（Halofuginone, HF）对野生型细胞与GCN2敲低细胞中肿瘤坏死因子（TNF）诱导的炎症基因表达的影响，并对经TNF-α（肿瘤坏死因子α）处理、同时存在或不存在哈夫格鲁宁（HF）的原发性类风湿关节炎成纤维样滑膜细胞（rheumatoid arthritis fibroblast-like synoviocytes, RA-FLS）开展了RNA测序（RNA-seq）分析。为探究氨酰tRNA合成酶（aminoacyl tRNA synthetase, AARS）抑制剂HF对RA-FLS炎症应答的影响，本研究对培养细胞进行如下处理：每个实验条件均设置重复样本，先用HF处理细胞16小时，再以TNF-α处理8或24小时。