Deletion of TECRL promotes skeletal muscle repair by up-regulating EGR2
Sha Geng, Songbai Liu, Wei He, Xiangbin Pan, Yi Sun, Ting Xue, S.H. Han, Jing Lou, Ying Chang, Jiqing Zheng, X. Shi, Yangxin Li, Yao‐Hua Song
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.