Endothelial cell signature in muscle stem cells validated by VEGFA-FLT1-AKT1 axis promoting survival of muscle stem cell.
Mayank VermaYoko AsakuraXuerui WangKasey ZhouMahmut ÜnverdiAllison P KannRobert S KraussAtsushi AsakuraPublished in: eLife (2024)
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.
Keyphrases
- stem cells
- single cell
- signaling pathway
- rna seq
- skeletal muscle
- endothelial cells
- acute myeloid leukemia
- induced apoptosis
- tyrosine kinase
- genome wide
- cell therapy
- pi k akt
- poor prognosis
- cell proliferation
- high throughput
- free survival
- epithelial mesenchymal transition
- cell cycle arrest
- high glucose
- dendritic cells
- type diabetes
- deep learning
- big data
- mesenchymal stem cells
- endoplasmic reticulum stress
- machine learning
- cell death
- vascular endothelial growth factor
- type iii