Setd2 reprograns lipid metabolism for the resolution of inflammation via H3K36me3 modification

Purpose: The goal of this study is to identify differential Setd2-mediated H3K36me3 modificaion in the resolution phase of inflammation induced by LPS Methods: We profiled chip-seq with H3K36me3 antibody in bone marrow-derived macrophages stimulated with LPS for 0h, 4h, 16h. Results: We find different H3K36me3 enrichment peaks under LPS stimulation at different time. BMDMs were stimulated with LPS for 0h, 4h, 16h, and then subjected to ChIP-seq.

研究目的：本研究旨在鉴定脂多糖（LPS）诱导的炎症消退阶段中，Setd2介导的H3K36me3修饰差异。实验方法：我们采用H3K36me3抗体，对分别经脂多糖（LPS）刺激0、4、16小时的骨髓源性巨噬细胞（bone marrow-derived macrophages, BMDMs）开展染色质免疫共沉淀测序（ChIP-seq）分析。实验结果：我们发现脂多糖刺激的不同时间点下存在差异的H3K36me3富集峰。将骨髓源性巨噬细胞经脂多糖刺激0、4、16小时后，进行染色质免疫共沉淀测序。