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Transcriptomic analysis of total plantaris muscles RNA extract before and after one week of overload

ABSTRACT: Adult skeletal muscle is a plastic tissue that can adapt its size to workload. Here, we show that RhoA within myofibers is needed for overload-induced hypertrophy by controlling satellite cell fusion to the growing myofibers without affecting protein synthesis. At the molecular level, we demonstrate that, in response to increased workload, RhoA controls in a cell autonomous manner Erk1/2 activation and the expressions of extracellular matrix (ECM) regulators such as Mmp9/Mmp13/Adam8 and of macrophage chemo-attractants such as Ccl3/Cx3cl1. Their decreased expression in RhoA mutant is associated with ECM and fibrillar collagen disorganization and lower macrophage infiltration. Moreover, Mmps inhibition and macrophage depletion in controls phenocopied the lack of growth of RhoA mutants. These findings unravel the implication of RhoA within myofibers, in response to increase load, in the building of a permissive microenvironment for muscle growth and for satellite cell accretion through ECM remodeling and inflammatory cell recruitment.

ORGANISM(S): Mus musculus

PROVIDER: GSE166597 | GEO | 2021/12/21

REPOSITORIES: GEO

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Transcriptomic analysis of differentiated myoblasts

Project description:Adult skeletal muscle is a plastic tissue that can adapt its size to workload. Here, we show that RhoA within myofibers is needed for overload-induced hypertrophy by controlling satellite cell fusion to the growing myofibers without affecting protein synthesis. At the molecular level, we demonstrate that, in response to increased workload, RhoA controls in a cell autonomous manner Erk1/2 activation and the expressions of extracellular matrix (ECM) regulators such as Mmp9/Mmp13/Adam8 and of macrophage chemo-attractants such as Ccl3/Cx3cl1. Their decreased expression in RhoA mutant is associated with ECM and fibrillar collagen disorganization and lower macrophage infiltration. Moreover, Mmps inhibition and macrophage depletion in controls phenocopied the lack of growth of RhoA mutants. These findings unravel the implication of RhoA within myofibers, in response to increase load, in the building of a permissive microenvironment for muscle growth and for satellite cell accretion through ECM remodeling and inflammatory cell recruitment.

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transcriptomic analysis of proliferative or differentiated myoblasts

Project description:Adult skeletal muscle is a plastic tissue that can adapt its size to workload and that can regenerate after demage. Here, we show that RhoA within primary myoblasts is needed for a correct muscle regeneration by controlling satellite cell fusion without affecting their proliferation or their differentiation. Moreover primary cultured myoblast loosing RhoA have no defects in cytoskeleton reorganization however their movement is altered compared to control cells. At the molecular level, we found that RhoA controls the expressions of different genes depending on step of differentiation process, not necessarly already described as implicated in fusion program. These findings unravel the implication of RhoA within satellite cells regulating myoblast fusion in response to demage in order to allow a correct regeneration process.

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Transcription profiling of mouse satellite cells isolated from skeletal muscle

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Sex hormones establish a reserve pool of adult muscle stem cells at puberty

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Fibronectin regulates Wnt7a signaling and satellite cell expansion

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