PMID- 20108254
OWN - NLM
STAT- MEDLINE
DCOM- 20100629
LR  - 20191210
IS  - 1097-4644 (Electronic)
IS  - 0730-2312 (Linking)
VI  - 109
IP  - 6
DP  - 2010 Apr 15
TI  - Physcion-8-O-beta-D-glucopyranoside enhances the commitment of mouse mesenchymal 
      progenitors into osteoblasts and their differentiation: Possible involvement of 
      signaling pathways to activate BMP gene expression.
PG  - 1148-57
LID - 10.1002/jcb.22494 [doi]
AB  - Here, we show the involvement of signaling pathways to induce the gene expression 
      of bone morphogenetic protein (BMP) in the osteogenic activity of 
      physcion-8-O-beta-D-glucopyranoside (physcion-Glu); it stimulated osteoblast 
      differentiation in mouse osteoblast MC3T3-E1 subclone 4 cells and induced BMP-2 
      gene expression and activation of Akt and ERK/MAP kinases. Physcion-Glu-induced 
      BMP-2 expression and mineralization were attenuated by LY294002, an inhibitor of 
      PI3K that lies upstream of Akt and MAP kinases, suggesting that physcion-Glu 
      induces osteoblast differentiation via PI3K-Akt/MAP kinase signaling pathways, 
      which play important roles in inducing BMP-2 gene expression. Physcion-Glu also 
      enhanced BMP-2-induced commitment of mouse bi-potential mesenchymal precursor 
      C2C12 cells into osteoblasts while inducing the transcription of several 
      osteogenic BMP isoforms, such as BMP-2, -4, -7, and -9. Osteogenic synergy 
      between BMP-2 and physcion-Glu was supported by the fact that noggin inhibited 
      BMP-2 and physcion-Glu-induced alkaline phosphatase expression and activity. 
      Considering that physcion-Glu induced Runx2 activity and the nuclear 
      translocation of p-Smad, physcion-Glu could act by enhancing the BMP signaling 
      pathway that induces Smad activation and translocation to activate Runx2. In 
      conclusion, physcion-Glu could enhance the commitment of mesenchymal progenitors 
      into osteoblasts and their differentiation by activating signaling pathways to 
      induce BMP gene expression.
FAU - Lee, Su-Ui
AU  - Lee SU
AD  - Laboratory of Chemical Genomics, Korea Research Institute of Chemical Technology, 
      Daejeon 305-600, Korea.
FAU - Choi, Yeon Hee
AU  - Choi YH
FAU - Kim, Young Sup
AU  - Kim YS
FAU - Park, Sang-Joon
AU  - Park SJ
FAU - Kwak, Han Bok
AU  - Kwak HB
FAU - Min, Yong Ki
AU  - Min YK
FAU - Kim, Hyun-Nam
AU  - Kim HN
FAU - Lim, Kyung-Eun
AU  - Lim KE
FAU - Choi, Je-Yong
AU  - Choi JY
FAU - Rhee, Myungchull
AU  - Rhee M
FAU - Kim, Seong Hwan
AU  - Kim SH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (Bmp2 protein, mouse)
RN  - 0 (Bone Morphogenetic Protein 2)
RN  - 0 (Chromones)
RN  - 0 (Glucosides)
RN  - 0 (Morpholines)
RN  - 0 (Phosphoinositide-3 Kinase Inhibitors)
RN  - 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one)
RN  - H6PT94IV61 (physcione)
RN  - KA46RNI6HN (Emodin)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Bone Morphogenetic Protein 2/genetics/*metabolism
MH  - Cell Differentiation/drug effects
MH  - Cell Line
MH  - Chromones/pharmacology
MH  - Emodin/*analogs & derivatives/chemistry
MH  - Glucosides/*chemistry/*pharmacology
MH  - Mesenchymal Stem Cells/*cytology/*drug effects
MH  - Mice
MH  - Morpholines/pharmacology
MH  - Osteoblasts/*cytology
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Phosphoinositide-3 Kinase Inhibitors
MH  - Polymerase Chain Reaction
MH  - Promoter Regions, Genetic/genetics
MH  - Signal Transduction/*drug effects
EDAT- 2010/01/29 06:00
MHDA- 2010/06/30 06:00
CRDT- 2010/01/29 06:00
PHST- 2010/01/29 06:00 [entrez]
PHST- 2010/01/29 06:00 [pubmed]
PHST- 2010/06/30 06:00 [medline]
AID - 10.1002/jcb.22494 [doi]
PST - ppublish
SO  - J Cell Biochem. 2010 Apr 15;109(6):1148-57. doi: 10.1002/jcb.22494.