Homeobox protein MSX-1 inhibits expression of bone morphogenetic protein 2, bone morphogenetic protein 4, and lymphoid enhancer-binding factor 1 via Wnt/β-catenin signaling to prevent differentiation of dental mesenchymal cells during the late bell stage

2017 ◽  
Vol 126 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Xiao-Yu Feng ◽  
Xiao-Shan Wu ◽  
Jin-Song Wang ◽  
Chun-Mei Zhang ◽  
Song-Lin Wang
Keyword(s):  
Bone Morphogenetic Protein ◽  
Mesenchymal Cells ◽  
Bone Morphogenetic Protein 2 ◽  
Bone Morphogenetic Protein 4 ◽  
Morphogenetic Protein ◽  
Binding Factor ◽  
Homeobox Protein

scholarly journals Differential Roles of Smad1 and p38 Kinase in Regulation of Peroxisome Proliferator-activating Receptor γ during Bone Morphogenetic Protein 2-induced Adipogenesis

2003 ◽  
Vol 14 (2) ◽  
pp. 545-555 ◽  
Author(s):  
Kenji Hata ◽  
Riko Nishimura ◽  
Fumiyo Ikeda ◽  
Kenji Yamashita ◽  
Takuma Matsubara ◽  
...  
Keyword(s):  
Bone Morphogenetic Protein ◽  
Transcriptional Activity ◽  
Mesenchymal Cells ◽  
Bone Morphogenetic Protein 2 ◽  
Peroxisome Proliferator ◽  
P38 Kinase ◽  
Morphogenetic Protein ◽  
Adipocytic Differentiation ◽  
Pparγ Expression ◽  
Activating Receptor

Bone morphogenetic protein 2 (BMP2) promotes the differentiation of undifferentiated mesenchymal cells into adipocytes. To investigate the molecular mechanisms that regulate this differentiation process, we studied the relationship between BMP2 signaling and peroxisome proliferator-activating receptor γ (PPARγ) during adipogenesis of mesenchymal cells by using pluripotent mesenchymal cell line C3H10T1/2. In C3H10T1/2 cells, BMP2 induced expression of PPARγ along with adipogenesis. Overexpression of Smad6, a natural antagonist for Smad1, blocked PPARγ expression and adipocytic differentiation induced by BMP2. Overexpression of dominant-negative PPARγ also diminished adipocytic differentiation of C3H10T1/2 cells, suggesting the central role of PPARγ in BMP2-induced adipocytic differentiation. Specific inhibitors for p38 kinase inhibited BMP2-induced adipocytic differentiation and transcriptional activation of PPARγ, whereas overexpression of Smad6 had no effect on transcriptional activity of PPARγ. Furthermore, activation of p38 kinase by overexpression of TAK1 and TAB1, without affecting PPARγ expression, led the up-regulation of transcriptional activity of PPARγ. These results suggest that both Smad and p38 kinase signaling are concomitantly activated and responsible for BMP2-induced adipocytic differentiation by inducing and up-regulating PPARγ, respectively. Thus, BMP2 controls adipocytic differentiation by using two distinct signaling pathways that play differential roles in this process in C3H10T1/2 cells.

scholarly journals Turning Bone Morphogenetic Protein 2 (BMP2) on and off in Mesenchymal Cells

2015 ◽  
Vol 116 (10) ◽  
pp. 2127-2138 ◽  
Author(s):  
Melissa B. Rogers ◽  
Tapan A. Shah ◽  
Nadia N. Shaikh
Keyword(s):  
Bone Morphogenetic Protein ◽  
Mesenchymal Cells ◽  
Bone Morphogenetic Protein 2 ◽  
Morphogenetic Protein

scholarly journals An osteogenesis-related transcription factor, core-binding factor A1, is constitutively expressed in the chondrocytic cell line TC6, and its expression is upregulated by bone morphogenetic protein-2

2000 ◽  
Vol 165 (3) ◽  
pp. 579-586 ◽  
Author(s):  
Y Takazawa ◽  
K Tsuji ◽  
A Nifuji ◽  
H Kurosawa ◽  
Y Ito ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Line ◽  
Bone Morphogenetic Protein ◽  
Blot Analysis ◽  
Bone Morphogenetic Protein 2 ◽  
Type I ◽  
Dependent Manner ◽  
Core Binding Factor ◽  
Morphogenetic Protein ◽  
Binding Factor

Core-binding factor A1 (Cbfa1), also called Pebp2 alpha A/AML3, is a transcription factor that belongs to the runt-domain gene family. Cbfa1-deficient mice are completely incapable of both endochondral and intramembranous bone formation, indicating that Cbfa1 is indispensable for osteogenesis. Maturation of chondrocytes in these mice is also disorganized, suggesting that Cbfa1 may also play a role in chondrogenesis. The aim of this study was to examine the expression and regulation of Pebp2 alpha A/AML3/Cbfa1 expression in the chondrocyte-like cell line, TC6. Northern blot analysis indicated that Cbfa1 mRNA was constitutively expressed as a 6.3 kb message in TC6 cells and the level of Cbfa1 expression was enhanced by treatment with bone morphogenetic protein-2 (BMP2) in a time- and dose-dependent manner. This effect was blocked by an RNA polymerase inhibitor, 5,6-dichloro-1-beta-d-ribofuranosylbenzimidazole, but not by a protein synthesis inhibitor, cycloheximide. Western blot analysis of the cell lysates using polyclonal antibody raised against Cbfa1 indicated that BMP2 treatment increased the Cbfa1 protein level in TC6 cells. In TC6 cells, BMP2 treatment enhanced expression of alkaline phosphatase and type I collagen mRNAs but suppressed that of type II collagen mRNA. In addition to TC6 cells, Cbfa1 mRNA was also expressed in primary cultures of chondrocytes and BMP2 treatment enhanced Cbfa1 mRNA expression in these cells similarly to its effect on TC6 cells. These data indicate that the Pebp2 alpha A/AML3/Cbfa1 gene is expressed in a chondrocyte-like cell line, TC6, and its expression is enhanced by treatment with BMP.

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