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<p>It is widely acknowledged that articular cartilage lacks the ability to regenerate. However, if such regeneration were possible, which cell type would generate new tissue? The <i>p21</i><sup>−/−</sup> mouse provides an excellent platform to explore this question, hence, we conducted lineage tracing on Paired related homeobox 1 (Prrx1/Prx1) cells post-injury to determine whether endogenous <i>Prx1</i><sup>+</sup> cells contribute to regenerated tissues post-injury. <i>p21</i><sup>−/−</sup> mice displayed enhanced endogenous cartilage regeneration, accompanied by notable differences in the number and kinetics of <i>Prx1</i><sup>+</sup> cells within and around the injury site. In <i>p21</i><sup>−/−</sup> mice, <i>Prx1</i><sup>+</sup> cells underwent chondrogenesis, ultimately contributing to the regenerated articular cartilage layer. These findings underscore the impact of tissue-resident cells on cartilage regeneration, albeit under abnormal conditions. If the conditions within the joint could be manipulated to favor such a regenerative environment, these endogenous cell types might be recruited to facilitate the formation of a new articular cartilage surface post-injury.</p>

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Prx1+ progenitors give rise to new articular cartilage when conditions are permissive for endogenous regeneration

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月9日

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  • Christina L. Jablonski,
  • Dora Modrcin,
  • John Cobb,
  • Donna-Marie McCafferty,
  • Paul T. Salo,
  • Roman J. Krawetz

摘要

It is widely acknowledged that articular cartilage lacks the ability to regenerate. However, if such regeneration were possible, which cell type would generate new tissue? The p21−/− mouse provides an excellent platform to explore this question, hence, we conducted lineage tracing on Paired related homeobox 1 (Prrx1/Prx1) cells post-injury to determine whether endogenous Prx1+ cells contribute to regenerated tissues post-injury. p21−/− mice displayed enhanced endogenous cartilage regeneration, accompanied by notable differences in the number and kinetics of Prx1+ cells within and around the injury site. In p21−/− mice, Prx1+ cells underwent chondrogenesis, ultimately contributing to the regenerated articular cartilage layer. These findings underscore the impact of tissue-resident cells on cartilage regeneration, albeit under abnormal conditions. If the conditions within the joint could be manipulated to favor such a regenerative environment, these endogenous cell types might be recruited to facilitate the formation of a new articular cartilage surface post-injury.