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p21-/- Mice Exhibit Spontaneous Articular Cartilage Regeneration Post-Injury
Christina L Jablonski1,2, Bryce A Besler1,2, Jahaan Ali1
1McCaig Institute for Bone & Joint Health, University of Calgary, Calgary, Alberta, Canada.
Objective:
Recent studies have implicated the cyclin dependent kinase inhibitor, p21, in enhanced tissue regeneration observed in MRL/MpJ "super-healer" mice. Specifically, p21 is downregulated in MRL cells and similar ear hole closure to MRL mice has been observed in p21-/- mice. However, the direct implications of p21 deletion in endogenous articular cartilage regeneration remain unknown. In this study, we investigated the role of p21 deletion in the ability of mice to heal full-thickness cartilage defects (FTCDs).
Design:
C57BL/6 and p21-/- (Cdkn1atm1Tyj) mice were subjected to FTCD and assessment of cartilage healing was performed at 1 hour, 3 days, 1 week, 2 weeks, and 4 weeks post-FTCD using a 14-point histological scoring system. X-ray microscopy was used to quantify cartilage healing parameters (e.g., cartilage thickness, surface area/volume) between C57BL/6 and p21-/- mice.
Results:
Absence of p21 resulted in increased spontaneous articular cartilage regeneration by 3 days post-FTCD. Furthermore, p21-/- mice presented with increased cartilage thickness at 1 and 2 weeks post-FTCD compared with uninjured controls, returning to baseline by 4 weeks post-FTCD.
Conclusions:
We report that p21-/- mice display enhanced articular cartilage regeneration post-FTCD compared with C57BL/6 mice. Furthermore, cartilage thickness was increased in p21-/- mice at 1 week post-FTCD compared with uninjured p21-/- mice and C57BL/6 mice.
Insights
Deleting p21 (cyclin dependent kinase inhibitor) enhances articular cartilage regeneration in mice after injury. P21 knockout mice showed improved healing and increased cartilage thickness, suggesting a role for p21 in cartilage repair.
Area of Science:
- Biomedical Science
- Regenerative Medicine
- Orthopedics
Background:
- The cyclin dependent kinase inhibitor, p21, is implicated in tissue regeneration.
- p21 is downregulated in MRL/MpJ mice, known for enhanced healing.
- The role of p21 in articular cartilage regeneration is not fully understood.
Purpose of the Study:
- To investigate the role of p21 deletion in endogenous articular cartilage regeneration.
- To assess the impact of p21 deficiency on healing full-thickness cartilage defects (FTCDs).
Main Methods:
- C57BL/6 and p21 knockout (p21-/-) mice underwent FTCD.
- Histological scoring (14-point system) assessed cartilage healing at multiple time points (1 hour to 4 weeks).
- X-ray microscopy quantified cartilage healing parameters (thickness, surface area/volume).
Main Results:
- Absence of p21 led to increased spontaneous articular cartilage regeneration by 3 days post-FTCD.
- p21-/- mice showed increased cartilage thickness at 1 and 2 weeks post-FTCD compared to controls.
- Cartilage thickness in p21-/- mice returned to baseline by 4 weeks post-FTCD.
Conclusions:
- p21 knockout mice exhibit enhanced articular cartilage regeneration following FTCD.
- p21 deficiency promotes cartilage repair, evidenced by increased cartilage thickness post-injury.
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