Primary cilia support cartilage regeneration after injury.
10.1038/s41368-023-00223-6
- Author:
Dike TAO
1
;
Lei ZHANG
1
;
Yunpeng DING
1
;
Na TANG
2
;
Xiaoqiao XU
1
;
Gongchen LI
3
;
Pingping NIU
1
;
Rui YUE
4
;
Xiaogang WANG
5
;
Yidong SHEN
2
;
Yao SUN
6
Author Information
1. Department of Implantology, School & Hospital of Stomatology, Tongji University, Shanghai, China.
2. State Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, China.
3. Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Shanghai, China.
4. Institute for Regenerative Medicine, Shanghai East Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
5. Key Laboratory of Big Data-Based Precision Medicine, School of Engineering Medicine, Beihang University, Beijing, China.
6. Department of Implantology, School & Hospital of Stomatology, Tongji University, Shanghai, China. yaosun@tongji.edu.cn.
- Publication Type:Research Support, Non-U.S. Gov't
- MeSH:
Mice;
Animals;
Hedgehog Proteins/genetics*;
Receptors, G-Protein-Coupled/metabolism*;
Cilia/metabolism*;
Cartilage/metabolism*;
Regeneration
- From:
International Journal of Oral Science
2023;15(1):22-22
- CountryChina
- Language:English
-
Abstract:
In growing children, growth plate cartilage has limited self-repair ability upon fracture injury always leading to limb growth arrest. Interestingly, one type of fracture injuries within the growth plate achieve amazing self-healing, however, the mechanism is unclear. Using this type of fracture mouse model, we discovered the activation of Hedgehog (Hh) signaling in the injured growth plate, which could activate chondrocytes in growth plate and promote cartilage repair. Primary cilia are the central transduction mediator of Hh signaling. Notably, ciliary Hh-Smo-Gli signaling pathways were enriched in the growth plate during development. Moreover, chondrocytes in resting and proliferating zone were dynamically ciliated during growth plate repair. Furthermore, conditional deletion of the ciliary core gene Ift140 in cartilage disrupted cilia-mediated Hh signaling in growth plate. More importantly, activating ciliary Hh signaling by Smoothened agonist (SAG) significantly accelerated growth plate repair after injury. In sum, primary cilia mediate Hh signaling induced the activation of stem/progenitor chondrocytes and growth plate repair after fracture injury.
