A Tead1-Apelin axis directs paracrine communication from myogenic to endothelial cells in skeletal muscle.

ABSTRACT: Apelin (Apln) is a myokine that regulates skeletal muscle plasticity and metabolism and declines during aging. Through a yeast one-hybrid transcription factor binding screen, we identified the TEA domain transcription factor 1 (Tead1) as a novel regulator of the Apln promoter. Single-cell analysis of regenerating muscle revealed that the apelin receptor (Aplnr) is enriched in endothelial cells, whereas Tead1 is enriched in myogenic cells. Knock-down of Tead1 stimulates Apln secretion from muscle cells in vitro and myofiber-specific overexpression of Tead1 suppresses Apln secretion in vivo. Apln secretion via Tead1 knock-down in muscle cells stimulates endothelial cell expansion via endothelial Aplnr. In vivo, Apln peptide suppl

SUBMITTER: Lee U 

PROVIDER: S-EPMC9250016 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature