Open AccessPromotion of Ccn2 expression and osteoblastic differentiation by actin polymerization, which is induced by laminar fluid flow stress
Author(s) -
Honjo Tadashi,
Kubota Satoshi,
Kamioka Hiroshi,
Sugawara Yasuyo,
Ishihara Yoshihito,
Yamashiro Takashi,
Takigawa Masaharu,
TakanoYamamoto Teruko
Publication year - 2012
Publication title -
journal of cell communication and signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 44
eISSN - 1873-961X
pISSN - 1873-9601
DOI - 10.1007/s12079-012-0177-z
Subject(s) - cytochalasin d , stress fiber , microbiology and biotechnology , chemistry , rho associated protein kinase , actin , signal transduction , rho kinase inhibitor , actin cytoskeleton , biophysics , cytoskeleton , cell , biology , biochemistry , focal adhesion
Fluid flow stress (FSS) is a major mechanical stress that induces bone remodeling upon orthodontic tooth movement, whereas CCN family protein 2 (CCN2) is a potent regenerator of bone defects. In this study, we initially evaluated the effect of laminar FSS on Ccn2 expression and investigated its mechanism in osteoblastic MC3T3‐E1 cells. The Ccn2 expression was drastically induced by uniform FSS in an intensity dependent manner. Of note, the observed effect was inhibited by a Rho kinase inhibitor Y27632. Moreover, the inhibition of actin polymerization blocked the FSS‐induced activation of Ccn2 , whereas inducing F‐actin formation using cytochalasin D and jasplakinolide enhanced Ccn2 expression in the same cells. Finally, F‐actin formation was found to induce osteoblastic differentiation. In addition, activation of cyclic AMP‐dependent kinase, which inhibits Rho signaling, abolished the effect of FSS . Collectively, these findings indicate the critical role of actin polymerization and Rho signaling in CCN2 induction and bone remodeling provoked by FSS.