Related Experiment Video
Updated: Aug 10, 2025
Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
Published on: April 1, 2022
NLRP3 Regulates Mandibular Healing through Interaction with UCHL5 in MSCs
Wenhua Zhao1,2, Yanan Cao1,2, Yue Chen1
1Department of Basic Science of Stomatology, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing, China; Jiangsu Province Key Laboratory of Oral Diseases, Nanjing, China; Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing, China.
NLRP3 inflammasome activation negatively impacts mandibular healing by inhibiting bone formation and osteoblast differentiation. Targeting NLRP3 or its regulator UCHL5 promotes healing and bone regeneration.
Area of Science:
- Biomedical Science
- Regenerative Medicine
- Oral and Maxillofacial Surgery
Background:
- The NLRP3 inflammasome plays roles in various physiological and pathological processes.
- The specific function and activation mechanism of NLRP3 in mandibular healing are not well understood.
Purpose of the Study:
- To investigate the role and mechanism of NLRP3 inflammasome activation in mandibular healing.
- To identify regulators of NLRP3 in this process.
Main Methods:
- Established a full-thickness mandibular defect model in wild-type and Prx1-Cre/ROSAnTnG mice.
- Assessed NLRP3 activation in mesenchymal stem cells (MSCs) during healing.
- Investigated the effect of NLRP3 inhibition and identified UCHL5 as a key regulator.
Main Results:
- NLRP3 was activated in MSCs during mandibular healing, particularly in Prx1+ cells.
- Inhibiting NLRP3 enhanced bone formation and osteoblast differentiation.
- UCHL5 was identified as a regulator that stabilizes NLRP3 via the ubiquitin-proteasome pathway.
- UCHL5 inhibition promoted NLRP3 ubiquitination and degradation, enhancing osteoblast differentiation.
Conclusions:
- NLRP3 acts as a negative modulator in mandibular healing.
- UCHL5 stabilizes NLRP3, and its inhibition promotes mandibular healing by enhancing NLRP3 degradation.
- These findings offer new insights into the post-translational modification of NLRP3 and its role in bone regeneration.
