AR cooperates with SMAD4 to maintain muscle homeostasis

The goal of this study was to determine the mechanism of androgne in driving muscle hypertrophy programmes. CONCLUSION: AR transcriptionally cooperates with SMAD4 and this affect is lost in the presence of expansion of the polyglutamine repeat in the AR gene. RNA-seq was performed in quadricpes femoris from SBMA (spinal bulbar muscular atrophy) AR100Q mice treated with AAV vectors expressing BMP7 or GFP mock control. Untreated wild-type mice (C57BL/6) were analysed in parallel as additional controls.

本研究旨在明确雄激素（androgen）介导肌肉肥大程序的作用机制。结论：雄激素受体（Androgen Receptor，AR）可与SMAD4发生转录协同作用，当AR基因中存在多聚谷氨酰胺重复序列扩增时，该协同效应将消失。本研究对经表达骨形态发生蛋白7（Bone Morphogenetic Protein 7，BMP7）或绿色荧光蛋白（Green Fluorescent Protein，GFP）空白对照的腺相关病毒（Adeno-Associated Virus，AAV）载体处理的脊髓延髓肌萎缩症（spinal bulbar muscular atrophy，SBMA）AR100Q小鼠的股四头肌（Quadriceps Femoris）开展了RNA测序（RNA-seq）。同时将未处理的野生型C57BL/6小鼠作为额外对照进行平行分析。