mTORC1 signaling pathway regulates tooth repair.
10.1038/s41368-023-00218-3
- Author:
Honghong LIU
1
;
Yu YUE
1
;
Zhiyun XU
1
;
Li GUO
1
;
Chuan WU
2
;
Da ZHANG
2
;
Lingfei LUO
2
;
Wenming HUANG
1
;
Hong CHEN
1
;
Deqin YANG
3
Author Information
1. Department of Endodontics, Stomatological Hospital of Chongqing Medical University, Chongqing, China.
2. Institute of Developmental Biology and Regenerative Medicine, Southwest University, Chongqing, China.
3. Department of Endodontics, Stomatological Hospital of Chongqing Medical University, Chongqing, China. yangdeqin@hospital.cqmu.edu.cn.
- Publication Type:Research Support, Non-U.S. Gov't
- MeSH:
Animals;
Mice;
Mechanistic Target of Rapamycin Complex 1/pharmacology*;
Signal Transduction;
Tooth/metabolism*;
Tooth Germ/metabolism*;
Odontogenesis
- From:
International Journal of Oral Science
2023;15(1):14-14
- CountryChina
- Language:English
-
Abstract:
Tooth germ injury can lead to abnormal tooth development and even tooth loss, affecting various aspects of the stomatognathic system including form, function, and appearance. However, the research about tooth germ injury model on cellular and molecule mechanism of tooth germ repair is still very limited. Therefore, it is of great importance for the prevention and treatment of tooth germ injury to study the important mechanism of tooth germ repair by a tooth germ injury model. Here, we constructed a Tg(dlx2b:Dendra2-NTR) transgenic line that labeled tooth germ specifically. Taking advantage of the NTR/Mtz system, the dlx2b+ tooth germ cells were depleted by Mtz effectively. The process of tooth germ repair was evaluated by antibody staining, in situ hybridization, EdU staining and alizarin red staining. The severely injured tooth germ was repaired in several days after Mtz treatment was stopped. In the early stage of tooth germ repair, the expression of phosphorylated 4E-BP1 was increased, indicating that mTORC1 is activated. Inhibition of mTORC1 signaling in vitro or knockdown of mTORC1 signaling in vivo could inhibit the repair of injured tooth germ. Normally, mouse incisors were repaired after damage, but inhibition/promotion of mTORC1 signaling inhibited/promoted this repair progress. Overall, we are the first to construct a stable and repeatable repair model of severe tooth germ injury, and our results reveal that mTORC1 signaling plays a crucial role during tooth germ repair, providing a potential target for clinical treatment of tooth germ injury.
