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Orthodontic compressive force modulates Ets‐1/Tks5 pathway to promote the formation of circumferential invadopodia and the fusion of osteoclast precursors
Author(s) -
Wang Yifan,
Zeng Zhimin,
Cheng Yali,
Zhao Liyao,
Yan Qiqi,
Qiu Yu,
Hu Jiangtian,
Guo Jie
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27879
Subject(s) - osteoclast , invadopodia , downregulation and upregulation , microbiology and biotechnology , chemistry , materials science , biology , biochemistry , genetics , cancer , cancer cell , gene , in vitro
During orthodontic treatment a mechanical force is applied to the teeth. However, it remains unclear how mechanical force promotes the maturation and fusion of osteoclast precursors into osteoclasts. In this study, we aimed to explore the mechanism by which orthodontic compressive force promotes osteoclast maturation. We used a RAW264.7 macrophage‐like cell line derived from Balb/c mice as the experimental model. We found that compressive force promoted the maturation of osteoclasts based on tartrate‐resistant acid phosphatase staining and the formation of invadopodia based on immunstaining of Tks5 and F‐actin. Moreover, we found that compressive force upregulated the expression of Ets‐1 and Tks5 and promoted the activation of Ets‐1 in RAW264.7 cells. Furthermore, we identified Tks5 as a transcription target of Ets‐1 in RAW264.7 cells and demonstrated that Ets‐1 mediates the effects of compressive force on Tks5 upregulation, invadopodia formation and cell fusion in osteoclasts. In conclusion, Ets‐1 is upregulated by compressive force and it is essential to transducing the mechanical signal to promote invadopodia formation and osteoclast fusion. Our findings provide novel insight into the mechanism underlying osteoclast maturation and fusion during orthodontic treatment.