scholarly journals Parathyroid Hormone-Related Peptide Interacts with Bone Morphogenetic Protein 2 to Increase Osteoblastogenesis and Decrease Adipogenesis in Pluripotent C3H10T½ Mesenchymal Cells

Endocrinology ◽  
2003 ◽  
Vol 144 (12) ◽  
pp. 5511-5520 ◽  
Author(s):  
George K. Chan ◽  
Dengshun Miao ◽  
Ron Deckelbaum ◽  
Isabel Bolivar ◽  
Andrew Karaplis ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Bone Morphogenetic Protein ◽  
Mesenchymal Cells ◽  
Bone Morphogenetic Protein 2 ◽  
Related Peptide ◽  
Morphogenetic Protein ◽  
Parathyroid Hormone Related Peptide

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 Enhanced Bone Morphogenetic Protein-2-Induced Ectopic and Orthotopic Bone Formation by Intermittent Parathyroid Hormone (1–34) Administration

2010 ◽  
Vol 16 (12) ◽  
pp. 3769-3777 ◽  
Author(s):  
Diederik H.R. Kempen ◽  
Lichun Lu ◽  
Theresa E. Hefferan ◽  
Laura B. Creemers ◽  
Andras Heijink ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Bone Formation ◽  
Bone Morphogenetic Protein ◽  
Bone Morphogenetic Protein 2 ◽  
Morphogenetic Protein
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