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Updated: Sep 23, 2026

Identification and Analysis of Myogenic Progenitors In Vivo During Acute Skeletal Muscle Injury by High-Dimensional Single-Cell Mass Cytometry
11:02

Identification and Analysis of Myogenic Progenitors In Vivo During Acute Skeletal Muscle Injury by High-Dimensional Single-Cell Mass Cytometry

Published on: December 1, 2023

p21 is essential for normal myogenic progenitor cell function in regenerating skeletal muscle

T J Hawke1, A P Meeson, N Jiang

  • 1Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd., Dallas, TX 75390-8573, USA.

American Journal of Physiology. Cell Physiology
|June 27, 2003
PubMed

Insights

Mice lacking p21 (cyclin-dependent kinase inhibitor) show impaired skeletal muscle regeneration. This study reveals p21 is crucial for coordinating cell cycle exit and differentiation in myogenic progenitor cells (MPCs) for effective muscle repair.

Area of Science:

  • Muscle regeneration
  • Cell cycle regulation
  • Molecular biology

Background:

  • Myogenic progenitor cells (MPCs) are key to skeletal muscle regeneration.
  • The molecular mechanisms controlling MPC proliferation and differentiation remain largely unknown.
  • The role of cyclin-dependent kinase inhibitor p21 in muscle repair is unclear.

Purpose of the Study:

  • To investigate the role of p21 in skeletal muscle regeneration.
  • To determine if p21 deficiency enhances or impairs muscle repair.
  • To elucidate the effects of p21 on MPC proliferation, cell cycle progression, and differentiation.

Main Methods:

  • Utilized p21 knockout (p21-/-) and wild-type mice.
  • Induced skeletal muscle injury using cardiotoxin.
  • Assessed muscle regeneration, cell proliferation (PCNA), apoptosis (TUNEL), and MPC differentiation in vivo and in vitro.

Main Results:

  • Contrary to hypothesis, p21-/- mice exhibited attenuated skeletal muscle regeneration.
  • p21-/- muscle showed increased proliferation and apoptosis post-injury.
  • MPC differentiation was impaired in p21-/- mice, a cell-autonomous effect.
  • No compensatory changes in p27, p53, or p57 were observed.

Conclusions:

  • p21 is essential for coordinating cell cycle exit and differentiation in adult MPCs.
  • Absence of p21 significantly impairs skeletal muscle regeneration.
  • p21 plays a critical role in the molecular program of muscle repair.

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