Glycosylation of dentin matrix protein 1 is critical for fracture healing via promoting chondrogenesis.
10.1007/s11684-019-0693-9
- Author:
Hui XUE
1
;
Dike TAO
1
;
Yuteng WENG
1
;
Qiqi FAN
1
;
Shuang ZHOU
1
;
Ruilin ZHANG
1
;
Han ZHANG
2
;
Rui YUE
3
;
Xiaogang WANG
4
;
Zuolin WANG
5
;
Yao SUN
6
Author Information
1. Department of Implantology, School & Hospital of Stomatology, Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Shanghai, 200072, China.
2. School & Hospital of Stomatology, Tongji University, Shanghai, 200072, China.
3. School of Life Sciences and Technology, Tongji University, Shanghai, 200072, China.
4. Beijing Advanced Innovation Center for Big Data-Based Precision Medicine, Beihang University, Beijing, 100083, 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, 200072, China. zuolin@tongji.edu.cn.
6. Department of Implantology, School & Hospital of Stomatology, Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Shanghai, 200072, China. yaosun@tongji.edu.cn.
- Publication Type:Journal Article
- Keywords:
cartilage;
dentin matrix protein 1;
extracellular matrix;
fracture;
proteoglycan
- From:Frontiers of Medicine
2019;13(5):575-589
- CountryChina
- Language:English
-
Abstract:
Fractures are frequently occurring diseases that endanger human health. Crucial to fracture healing is cartilage formation, which provides a bone-regeneration environment. Cartilage consists of both chondrocytes and extracellular matrix (ECM). The ECM of cartilage includes collagens and various types of proteoglycans (PGs), which play important roles in maintaining primary stability in fracture healing. The PG form of dentin matrix protein 1 (DMP1-PG) is involved in maintaining the health of articular cartilage and bone. Our previous data have shown that DMP1-PG is richly expressed in the cartilaginous calluses of fracture sites. However, the possible significant role of DMP1-PG in chondrogenesis and fracture healing is unknown. To further detect the potential role of DMP1-PG in fracture repair, we established a mouse fracture model by using a glycosylation site mutant DMP1 mouse (S89G-DMP1 mouse). Upon inspection, fewer cartilaginous calluses and down-regulated expression levels of chondrogenesis genes were observed in the fracture sites of S89G-DMP1 mice. Given the deficiency of DMP1-PG, the impaired IL-6/JAK/STAT signaling pathway was observed to affect the chondrogenesis of fracture healing. Overall, these results suggest that DMP1-PG is an indispensable proteoglycan in chondrogenesis during fracture healing.
