PDF(Pubmed)
Abstract：
Myogenic regeneration relies on the proliferation and differentiation of satellite cells. TECRL (trans-2,3-enoyl-CoA reductase like) is an endoplasmic reticulum protein only expressed in cardiac and skeletal muscle. However, its role in myogenesis remains unknown. We show that TECRL expression is increased in response to injury. Satellite cell-specific deletion of TECRL enhances muscle repair by increasing the expression of EGR2 through the activation of the ERK1/2 signaling pathway, which in turn promotes the expression of PAX7. We further show that TECRL deletion led to the upregulation of the histone acetyltransferase general control nonderepressible 5, which enhances the transcription of EGR2 through acetylation. Importantly, we showed that AAV9-mediated TECRL silencing improved muscle repair in mice. These findings shed light on myogenic regeneration and muscle repair.
摘要：
生肌再生依赖于卫星细胞的增殖和分化。TECRL(反式-2,3-烯酰-CoA还原酶样)是仅在心肌和骨骼肌中表达的内质网蛋白。然而,其在肌生成中的作用尚不清楚。我们显示TECRL表达响应于损伤而增加。TECRL的卫星细胞特异性缺失通过激活ERK1/2信号通路增加EGR2的表达来增强肌肉修复，进而促进PAX7的表达。我们进一步表明，TECRL缺失导致组蛋白乙酰转移酶一般控制不可去抑制的5上调，从而通过乙酰化增强EGR2的转录。重要的是,我们发现AAV9介导的TECRL沉默能改善小鼠的肌肉修复。这些发现揭示了肌源性再生和肌肉修复。
