View : 44 Download: 0

PKC signaling inhibits osteogenic differentiation through the regulation of Msx2 function

Title
PKC signaling inhibits osteogenic differentiation through the regulation of Msx2 function
Authors
Jeong H.M.Jin Y.-H.Choi Y.H.Yum J.Choi J.-K.Yeo C.-Y.Lee K.-Y.
Ewha Authors
여창열
SCOPUS Author ID
여창열scopus
Issue Date
2012
Journal Title
Biochimica et Biophysica Acta - Molecular Cell Research
ISSN
0167-4889JCR Link
Citation
vol. 1823, no. 8, pp. 1225 - 1232
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Protein kinase C (PKC) signaling regulates osteoblast differentiation, but little is known about its downstream effectors. We examined the effect of modulating PKC activity on osteogenic transcription factors and found that the protein level of Msx2 is affected. Msx2 is induced by osteogenic signals such as BMPs and it plays critical roles in bone formation and osteoblast differentiation. Here, we examined the role of PKC signaling in regulating the function of Msx2. We found that the inhibition of PKC signaling enhances osteogenic differentiation in BMP2-stimulated C2C12 cells. Treatment with inhibitors of PKC activity or overexpression of kinase-defective (KD), dominant-negative mutant PKC isoforms strongly reduced the level of Msx2 protein. Several PKC isoforms (α, β, δ, and *) interacted with Msx2, and PKCβ phosphorylated Msx2 at Thr135 and Thr141. Msx2 repressed the transcriptional activity of the osteogenic transcription factor Runx2, and this repression was relieved by inhibition of PKC activity or overexpression of the KD mutant PKC isoforms. In addition, PKC prolonged the half-life of Msx2 protein. These results suggest that PKC signaling modulates osteoblast differentiation, at least in part, through the regulation of Msx2. © 2012 Elsevier B.V.
DOI
10.1016/j.bbamcr.2012.05.018
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE