Department of Pediatrics & Neurology, Division of Pediatric Neurology, The University of Texas Southwestern Medical Center, Dallas, United States.
Stem Cell Institute, University of Minnesota Medical School, Minneapolis, United States.
Elife. 2024 Jun 6;13:e73592. doi: 10.7554/eLife.73592.
Endothelial and skeletal muscle lineages arise from common embryonic progenitors. Despite their shared developmental origin, adult endothelial cells (ECs) and muscle stem cells (MuSCs; satellite cells) have been thought to possess distinct gene signatures and signaling pathways. Here, we shift this paradigm by uncovering how adult MuSC behavior is affected by the expression of a subset of EC transcripts. We used several computational analyses including single-cell RNA-seq (scRNA-seq) to show that MuSCs express low levels of canonical EC markers in mice. We demonstrate that MuSC survival is regulated by one such prototypic endothelial signaling pathway (VEGFA-FLT1). Using pharmacological and genetic gain- and loss-of-function studies, we identify the FLT1-AKT1 axis as the key effector underlying VEGFA-mediated regulation of MuSC survival. All together, our data support that the VEGFA-FLT1-AKT1 pathway promotes MuSC survival during muscle regeneration, and highlights how the minor expression of select transcripts is sufficient for affecting cell behavior.
内皮细胞和骨骼肌细胞系起源于共同的胚胎祖细胞。尽管它们具有共同的发育起源,但成年内皮细胞 (ECs) 和肌肉干细胞 (MuSCs; 卫星细胞) 被认为具有独特的基因特征和信号通路。在这里,我们通过揭示一部分 EC 转录本的表达如何影响成年 MuSC 的行为来改变这一范式。我们使用了几种计算分析方法,包括单细胞 RNA 测序 (scRNA-seq),以显示 MuSCs 在小鼠中低表达典型的 EC 标志物。我们证明 MuSC 的存活受到一种典型的内皮信号通路 (VEGFA-FLT1) 的调节。通过药理学和遗传功能获得和功能丧失研究,我们确定了 FLT1-AKT1 轴作为 VEGFA 介导的 MuSC 存活调节的关键效应物。总之,我们的数据支持 VEGFA-FLT1-AKT1 通路在肌肉再生过程中促进 MuSC 的存活,并强调了少数特定转录本的少量表达足以影响细胞行为。