Gli1(+) Cells Residing in Bone Sutures Respond to Mechanical Force via IP(3)R to Mediate Osteogenesis.
Gli1(+) Cells Residing in Bone Sutures Respond to Mechanical Force via IP(3)R to Mediate Osteogenesis.
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骨缝中的 Gli1( ) 细胞通过 IP3R 响应机械力以介导成骨
DOI：
10.1155/2021/8138374
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发表时间：
2021
影响因子：
4.3
通讯作者：
Jin Y
中科院分区：
文献类型：
--
作者：
Huang X;Li Z;Liu P;Wu M;Liu AQ;Hu C;Liu X;Guo H;Yang X;Guo X;Li B;He X;Xuan K;Jin Y
骨性错牙合畸形的早期正畸矫治利用机械力刺激未闭合缝的改建，促进骨重建，然而，其潜在机制仍不清楚。颌面骨缝中的Gli 1+细胞已被证明参与颌面骨发育和损伤修复。然而，这些细胞是否参与了正畸治疗过程中机械力诱导的骨重建仍有待研究。本研究利用两种能够标记Gli 1+细胞的转基因小鼠建立了快速上颌扩大（RME）小鼠模型和机械牵张负荷细胞模型，发现Gli 1+细胞在体内和体外均参与了机械力诱导的成骨过程。此外，我们发现机械力诱导的成骨通过肌醇1，4，5-三磷酸受体（IP 3R），我们首次观察到抑制Gli 1抑制机械力诱导的IP 3R过表达的增加，表明Gli 1+细胞通过IP 3R参与机械力诱导的成骨。总之，这项研究是第一个证明，Gli 1+细胞在颌面部缝参与机械力诱导的骨形成通过IP 3R在正畸治疗的骨骼错。此外，我们的研究结果提供了新的见解正畸治疗的机制，骨性错？
Early orthodontic correction of skeletal malocclusion takes advantage of mechanical force to stimulate unclosed suture remodeling and to promote bone reconstruction; however, the underlying mechanisms remain largely unclear. Gli1+ cells in maxillofacial sutures have been shown to participate in maxillofacial bone development and damage repair. Nevertheless, it remains to be investigated whether these cells participate in mechanical force-induced bone remodeling during orthodontic treatment of skeletal malocclusion. In this study, rapid maxillary expansion (RME) mouse models and mechanical stretch loading cell models were established using two types of transgenic mice which are able to label Gli1+ cells, and we found that Gli1+ cells participated in mechanical force-induced osteogenesis both in vivo and in vitro. Besides, we found mechanical force-induced osteogenesis through inositol 1,4,5-trisphosphate receptor (IP3R), and we observed for the first time that inhibition of Gli1 suppressed an increase in mechanical force-induced IP3R overexpression, suggesting that Gli1+ cells participate in mechanical force-induced osteogenesis through IP3R. Taken together, this study is the first to demonstrate that Gli1+ cells in maxillofacial sutures are involved in mechanical force-induced bone formation through IP3R during orthodontic treatment of skeletal malocclusion. Furthermore, our results provide novel insights regarding the mechanism of orthodontic treatments of skeletal malocclusion.
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影响因子：
5.6
作者：
Di Pietro, Lorena;Barba, Marta;Lattanzi, Wanda
通讯作者：
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影响因子：
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作者：
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DOI：
10.1016/j.coms.2019.08.006
发表时间：
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