LncRNA Nron regulates osteoclastogenesis during orthodontic bone resorption.
10.1038/s41368-020-0077-7
- Author:
Ruilin ZHANG
1
;
Junhui LI
1
;
Gongchen LI
1
;
Fujun JIN
2
;
Zuolin WANG
1
;
Rui YUE
3
;
Yibin WANG
3
;
Xiaogang WANG
4
;
Yao SUN
5
Author Information
1. Department of Implantology, School & Hospital of Stomatology, Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Shanghai, China.
2. School of Biological Science and Medical Engineering, Beihang University, Beijing, China.
3. School of Life Sciences and Technology, Tongji University, Shanghai, China.
4. School of Biological Science and Medical Engineering, Beihang University, Beijing, China. xiaogangwang@buaa.edu.cn.
5. Department of Implantology, School & Hospital of Stomatology, Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Shanghai, China. yaosun@tongji.edu.cn.
- Publication Type:Journal Article
- MeSH:
Animals;
Bone Resorption;
genetics;
Mice;
Mice, Inbred C57BL;
Osteoclasts;
Osteogenesis;
RANK Ligand;
RNA, Long Noncoding;
genetics
- From:
International Journal of Oral Science
2020;12(1):14-14
- CountryChina
- Language:English
-
Abstract:
Activation of osteoclasts during orthodontic tooth treatment is a prerequisite for alveolar bone resorption and tooth movement. However, the key regulatory molecules involved in osteoclastogenesis during this process remain unclear. Long noncoding RNAs (lncRNAs) are a newly identified class of functional RNAs that regulate cellular processes, such as gene expression and translation regulation. Recently, lncRNAs have been reported to be involved in osteogenesis and bone formation. However, as the most abundant noncoding RNAs in vivo, the potential regulatory role of lncRNAs in osteoclast formation and bone resorption urgently needs to be clarified. We recently found that the lncRNA Nron (long noncoding RNA repressor of the nuclear factor of activated T cells) is highly expressed in osteoclast precursors. Nron is downregulated during osteoclastogenesis and bone ageing. To further determine whether Nron regulates osteoclast activity during orthodontic treatment, osteoclastic Nron transgenic (Nron cTG) and osteoclastic knockout (Nron CKO) mouse models were generated. When Nron was overexpressed, the orthodontic tooth movement rate was reduced. In addition, the number of osteoclasts decreased, and the activity of osteoclasts was inhibited. Mechanistically, Nron controlled the maturation of osteoclasts by regulating NFATc1 nuclear translocation. In contrast, by deleting Nron specifically in osteoclasts, tooth movement speed increased in Nron CKO mice. These results indicate that lncRNAs could be potential targets to regulate osteoclastogenesis and orthodontic tooth movement speed in the clinic in the future.
