2022年8月5日，加拿大渥太华大学
研究人员证明了来自再生微环境的炎症细胞因子信号损害了静止的肌肉干细胞（MuSC）重新进入细胞周期的能力。组蛋白H3赖氨酸27（H3K27）去甲基化酶JMJD3，而不是UTX，允许MuSC克服抑制性炎症信号，通过去除Has2位点的三甲基化H3K27（H3K27me3）标记来启动透明质酸的生产，这反过来又建立了一个能够整合引导MuSC退出静止的信号的细胞外基质。因此，JMJD3驱动的透明质酸合成起着促进再生的作用，使MuSC适应炎症和启动肌肉修复。
据悉，MuSC居住在一个专门的微环境中，以确保其再生能力。虽然人们知道先天性免疫细胞会对损伤进行渗透，但目前仍不清楚MuSC如何适应这种改变了的环境来启动修复。
附：英文原文
Title: JMJD3 activated hyaluronan synthesis drives muscle regeneration in an inflammatory environment
Author: Kiran Nakka, Sarah Hachmer, Zeinab Mokhtari, Radmila Kovac, Hina Bandukwala, Clara Bernard, Yuefeng Li, Guojia Xie, Chengyu Liu, Magid Fallahi, Lynn A. Megeney, Julien Gondin, Bénédicte Chazaud, Marjorie Brand, Xiaohui Zha, Kai Ge, F. Jeffrey Dilworth
Issue&Volume: 2022-08-05
Abstract: Muscle stem cells (MuSCs) reside in a specialized niche that ensures their regenerative capacity. Although we know that innate immune cells infiltrate the niche in response to injury, it remains unclear how MuSCs adapt to this altered environment for initiating repair. Here, we demonstrate that inflammatory cytokine signaling from the regenerative niche impairs the ability of quiescent MuSCs to reenter the cell cycle. The histone H3 lysine 27 (H3K27) demethylase JMJD3, but not UTX, allowed MuSCs to overcome inhibitory inflammation signaling by removing trimethylated H3K27 (H3K27me3) marks at the Has2 locus to initiate production of hyaluronic acid, which in turn established an extracellular matrix competent for integrating signals that direct MuSCs to exit quiescence. Thus, JMJD3-driven hyaluronic acid synthesis plays a proregenerative role that allows MuSC adaptation to inflammation and the initiation of muscle repair.
DOI: abm9735
Source: https://www.science.org/doi/10.1126/science.abm9735