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TGF-beta2 stimulates cranial suture closure through activation of the Erk-MAPK pathway

Cited 30 time in Web of Science Cited 32 time in Scopus
Authors

Ryoo, Hyun-Mo; Lee, Sang-Won; Choi, Kang-Young; Cho, Je-Yoel; Jung, Sung-Hwa; Song, Kun-Bae; Park, Eui-Kyun; Choi, Je-Yong; Shin, Hong-In; Kim, Shin-Yoon; Woo, Kyung-Mi; Baek, Jeong-Hwa; Nam, Soon-Hyeun; Kim, Young-Jin; Kim, Hyun-Jung

Issue Date
2006-02
Publisher
Wiley-Blackwell
Citation
JOURNAL OF CELLULAR BIOCHEMISTRY 98:981-991
Abstract
Cranial sutures are important growth sites of the skull. During suture closure, the dura mater is one of the most important sources of various positive and negative regulatory signals. Previous results indicate that TGF-2 from dura mater strongly accelerates suture closure, however, its exact regulatory mechanism is still unclear. In this study, we confirmed that removal of dura mater in calvarial organ culture strongly accelerates sagittal suture closure and that this effect is further enhanced by TGF-2 treatment. TGF-2 stimulated cell proliferation in the MC3T3-E1 cell line. Similarly, it stimulated the proliferation of cells in the sutural space in calvarial organ culture. Furthermore, TGF-2-mediated enhanced cell proliferation and suture closure were almost completely inhibited by an Erk-MAPK blocker, PD98059. These results indicate that TGF-2-induced activation of Erk-MAPK is an important signaling component that stimulates cell proliferation to enrich osteoprogenitor cells, thereby promoting their differentiation into osteoblasts to achieve a rapid calvarial bone expansion. J. Cell. Biochem. 98: 981-991, 2006. © 2006 Wiley-Liss, Inc.
ISSN
0730-2312
Language
English
URI
https://hdl.handle.net/10371/69658
DOI
https://doi.org/10.1002/jcb.20773
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