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TGF‐β2 stimulates cranial suture closure through activation of the Erk‐MAPK pathway
Author(s) -
Lee SangWon,
Choi KangYoung,
Cho JeYoel,
Jung SungHwa,
Song KunBae,
Park EuiKyun,
Choi JeYong,
Shin HongIn,
Kim ShinYoon,
Woo KyungMi,
Baek JeongHwa,
Nam SoonHyeun,
Kim YoungJin,
Kim HyunJung,
Ryoo HyunMo
Publication year - 2006
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20773
Subject(s) - mapk/erk pathway , dura mater , sagittal suture , fibrous joint , cell growth , microbiology and biotechnology , skull , chemistry , transforming growth factor , anatomy , medicine , biology , signal transduction , biochemistry
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‐β2 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‐β2 treatment. TGF‐β2 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‐β2‐mediated enhanced cell proliferation and suture closure were almost completely inhibited by an Erk‐MAPK blocker, PD98059. These results indicate that TGF‐β2‐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.