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Decoding the transcriptome of denervated muscle at single-nucleus resolution.

Hongchun Lin1,2, Xinxin Ma1, Yuxiang Sun2

  • 1Nephrology Division, Department of Medicine, Baylor College of Medicine, Houston, TX, USA.

Journal of Cachexia, Sarcopenia and Muscle
|June 21, 2022
PubMed
Summary

Single-nucleus RNA sequencing reveals that denervation-induced muscle atrophy involves significant transcriptional reprogramming in specific myonuclei subtypes. This study uncovers key molecular changes underlying muscle plasticity and atrophy.

Keywords:
DenervationMuscle atrophyMuscle metabolismSkeletal musclesnRNA-seq

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Area of Science:

  • Molecular Biology
  • Genomics
  • Muscle Physiology

Background:

  • Skeletal muscle exhibits plasticity, with atrophy being an adaptive response to catabolic stimuli.
  • Heterogeneous transcriptome responses in muscle cells during catabolism are not fully understood.

Purpose of the Study:

  • To characterize muscle atrophy-related transcriptional changes at single-nucleus resolution using snRNA-seq.
  • To investigate the molecular basis of muscle cell heterogeneity and plasticity in response to catabolism.

Main Methods:

  • Single-nucleus RNA sequencing (snRNA-seq) on mouse gastrocnemius muscle from a sciatic denervation model.
  • Bioinformatics analyses including clustering, functional enrichment, trajectory analysis, and regulon inference.

Main Results:

  • Identified 13 nuclear types, with type IIb2 myonuclei showing increased proportion and significant transcriptional reprogramming upon denervation.
  • Discovered signature genes (e.g., Runx1, Gadd45a) and enhanced atrophy-related regulons (e.g., Foxo3, Runx1) in denervated type IIb2 myonuclei.
  • Observed down-regulation of most metabolic pathways, with specific activation of glutathione metabolism in denervated type IIb2 myonuclei and diminished cell-cell communication.

Conclusions:

  • Defined myonuclear transition, metabolic remodeling, and gene regulatory network reprogramming in denervation-induced muscle atrophy.
  • Illustrated the molecular mechanisms of muscle cell heterogeneity and plasticity during catabolism.
  • Provided a resource for further research into the molecular mechanisms of muscle atrophy.