Open AccessStretch-inducible Expression of Connective Tissue Growth Factor (CTGF) in Human Osteoblasts-like Cells is Mediated by PI3K-JNK Pathway
Author(s) -
Li-Wei Xiao,
Min Yang,
Jing Dong,
Hui Xie,
Guoliang Sui,
HE Yu-ling,
Jia-Xuan Lei,
LingQing Yuan,
Xiao Yuan
Publication year - 2011
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000331743
Subject(s) - ctgf , mapk/erk pathway , p38 mitogen activated protein kinases , growth factor , microbiology and biotechnology , connective tissue , pi3k/akt/mtor pathway , kinase , protein kinase a , signal transduction , mitogen activated protein kinase , chemistry , biology , biochemistry , receptor , genetics
To explore the possible role for connective tissue growth factor (CTGF) during tooth movement, we evaluated CTGF gene and protein expression in MG-63 cells subjected to cyclic stretch. Cyclic stretch caused a time-dependent increase in CTGF mRNA and protein levels.Inhibition of p38 MAP kinase or ERK activation did not affect cyclic stretch-induced CTGF expression. Specific inhibitors of PI3K suppressed stretch -induced CTGF expression in a time-dependent manner. cyclic stretch activated JNK and ERK, but not p38 MAP kinase in osteoblast-like cells. PI3K inhibitors suppressed cyclic stretch-induced JNK, but not p38 MAP kinase activation. Finally, SP600125, a Specific Inhibitor of JNK, suppressed stretch -induced CTGF Expression. These results suggest that stretch-induced CTGF expression is mediated through the PI3K-JNK -dependent pathway, not by p38 MAP kinase and ERK pathways.
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