Abstract:
:Bone mass is controlled by a balance between bone resorption and formation by osteoclasts and osteoblasts, respectively. An imbalance between osteoblasts and osteoclasts increases the risk of osteoporosis and fractures. Although inhibition of osteoclasts is beneficial for preventing and treating osteoporosis, enhanced bone formation through activation of osteoblast differentiation can be a more promising therapeutic approach. In this study, we attempted to isolate small molecules that promote osteoblast differentiation and found that IBIP (3-(2,3-dimethoxyphenyl)-1-[9-methyl-2-phenyl-9H-imidazo[1,2-a]benzimidazol-3-yl]-2-propen-1-one) was a potent activator of osteoblast differentiation. Upon bone morphogenetic protein-2 (BMP2) stimulation, IBIP promoted osteoblast differentiation and increased the expression of osteoblast-specific gene markers, such as osterix and alkaline phosphatase, in a dose-dependent manner. The phosphorylation of SMADs and extracellular signal-regulated kinase (ERK) increased after IBIP treatment. While enhanced SMAD phosphorylation by IBIP was abolished by a BMP inhibitor, IBIP-induced ERK phosphorylation was sustained in the presence of this inhibitor, but was decreased by an ERK kinase inhibitor. Suppression of IBIP-induced SMAD and ERK phosphorylation diminished osteoblast differentiation. Most importantly, IBIP enhanced bone formation and calcification in a BMP2-independent manner in vitro and advanced the skeletal development of zebrafish larvae in vivo. Collectively, IBIP may have beneficial effects on bone loss through potentiation of bone formation.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Bae SJ,Min YK,Hwang ESdoi
10.1016/j.bbrc.2017.04.075subject
Has Abstractpub_date
2017-05-27 00:00:00pages
409-414issue
2eissn
0006-291Xissn
1090-2104pii
S0006-291X(17)30751-9journal_volume
487pub_type
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