RRC ID 86433
著者 Zhang L, Saito H, Higashimoto T, Kaji T, Nakamura A, Iwamori K, Nagano R, Motooka D, Okuzaki D, Uezumi A, Seno S, Fukada SI.
タイトル Regulation of muscle hypertrophy through granulin: Relayed communication among mesenchymal progenitors, macrophages, and satellite cells.
ジャーナル Cell Rep
Abstract Skeletal muscles exert remarkable regenerative or adaptive capacities in response to injuries or mechanical loads. However, the cellular networks underlying muscle adaptation are poorly understood compared to those underlying muscle regeneration. We employed single-cell RNA sequencing to investigate the gene expression patterns and cellular networks activated in overloaded muscles and compared these results with those observed in regenerating muscles. The cellular composition of the 4-day overloaded muscle, when macrophage infiltration peaked, closely resembled that of the 10-day regenerating muscle. In addition to the mesenchymal progenitor-muscle satellite cell (MuSC) axis, interactome analyses or targeted depletion experiments revealed communications between mesenchymal progenitors-macrophages and macrophages-MuSCs. Furthermore, granulin, a macrophage-derived factor, inhibited MuSC differentiation, and Granulin-knockout mice exhibited blunted muscle hypertrophy due to the premature differentiation of overloaded MuSCs. These findings reveal the critical role of granulin through the relayed communications of mesenchymal progenitors, macrophages, and MuSCs in facilitating efficient muscle hypertrophy.
巻・号 43(4)
ページ 114052
公開日 2024-4-23
DOI 10.1016/j.celrep.2024.114052
PII S2211-1247(24)00380-2
PMID 38573860
MeSH Animals Cell Communication Cell Differentiation* Granulins Hypertrophy* Macrophages* / metabolism Male Mesenchymal Stem Cells* / metabolism Mice Mice, Inbred C57BL Mice, Knockout* Muscle, Skeletal / metabolism Muscle, Skeletal / pathology Regeneration Satellite Cells, Skeletal Muscle* / metabolism Satellite Cells, Skeletal Muscle* / pathology
IF 8.109
リソース情報
実験動物マウス RBRC02370