Effects of cortisol and bone morphogenetic protein-2 on stromal cell differentiation: correlation with CCAAT-enhancer binding protein expression

Bone ◽  
2002 ◽  
Vol 30 (5) ◽  
pp. 685-691 ◽  
Author(s):  
R.C. Pereira ◽  
A.M. Delany ◽  
E. Canalis
Keyword(s):  
Cell Differentiation ◽  
Protein Expression ◽  
Bone Morphogenetic Protein ◽  
Stromal Cell ◽  
Binding Protein ◽  
Bone Morphogenetic Protein 2 ◽  
Morphogenetic Protein ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein

scholarly journals CCAAT/Enhancer Binding Protein Homologous Protein (DDIT3) Induces Osteoblastic Cell Differentiation

Endocrinology ◽  
2004 ◽  
Vol 145 (4) ◽  
pp. 1952-1960 ◽  
Author(s):  
Renata C. Pereira ◽  
Anne M. Delany ◽  
Ernesto Canalis
Keyword(s):  
Bone Morphogenetic Protein ◽  
Stromal Cells ◽  
Binding Protein ◽  
Dominant Negative ◽  
Bone Morphogenetic Protein 2 ◽  
Smad Signaling ◽  
Homologous Protein ◽  
Morphogenetic Protein ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein

Abstract CCAAT/enhancer binding protein (C/EBP) homologous protein (CHOP/DDIT3), a member of the C/EBP family of transcription factors, plays a role in cell survival and differentiation. CHOP/DDIT3 binds to C/EBPs to form heterodimers that do not bind to consensus Cebp sequences, acting as a dominant-negative inhibitor. CHOP/DDIT3 blocks adipogenesis, and we postulated it could induce osteoblastogenesis. We investigated the effects of constitutive CHOP/DDIT3 overexpression in murine ST-2 stromal cells transduced with retroviral vectors. ST-2 cells differentiated toward osteoblasts, and CHOP/DDIT3 accelerated and enhanced the appearance of mineralized nodules, and the expression of osteocalcin and alkaline phosphatase mRNAs, particularly in the presence of bone morphogenetic protein-2. CHOP/DDIT3 overexpression opposed adipogenesis, and did not cause substantial changes in cell number. CHOP/DDIT3 overexpression did not modify C/EBPα or -β mRNA levels but decreased C/EBPδ after 24 d of culture. Electrophoretic mobility shift and supershift assays demonstrated that overexpression of CHOP/DDIT3 decreased the binding of C/EBPs to their consensus sequence by interacting with C/EBPα and -β, confirming its dominant-negative role. In addition, CHOP/DDIT3 enhanced bone morphogenetic protein-2/Smad signaling. In conclusion, CHOP/DDIT3 enhances osteoblastic differentiation of stromal cells, in part by interacting with C/EBPα and -β and also by enhancing Smad signaling.

scholarly journals Estrogen Regulates Amiloride-Binding Protein 1 through CCAAT/Enhancer-Binding Protein-β in Mouse Uterus during Embryo Implantation and Decidualization

Endocrinology ◽  
2010 ◽  
Vol 151 (10) ◽  
pp. 5007-5016 ◽  
Author(s):  
Xiao-Huan Liang ◽  
Zhen-Ao Zhao ◽  
Wen-Bo Deng ◽  
Zhen Tian ◽  
Wei Lei ◽  
...  
Keyword(s):  
Amine Oxidase ◽  
Binding Protein ◽  
Embryo Implantation ◽  
Bone Morphogenetic Protein 2 ◽  
Mouse Uterus ◽  
Morphogenetic Protein ◽  
Enhancer Binding Protein ◽  
Excess Amount ◽  
Ccaat Enhancer Binding Protein

Embryo implantation is an intricate interaction between receptive uterus and active blastocyst. The mechanism underlying embryo implantation is still unknown. Although histamine and putrescine are important for embryo implantation and decidualization, excess amount of histamine and putrescine is harmful. Amiloride binding protein 1 (Abp1) is a membrane-associated amine oxidase and mainly metabolizes histamine and putrescine. In this study, we first showed that Abp1 is strongly expressed in the decidua on d 5–8 of pregnancy. Abp1 expression is not detected during pseudopregnancy and under delayed implantation but is detected after estrogen activation. Because Abp1 is mainly localized in the decidua and also strongly expressed during in vitro decidualization, Abp1 might play a role during mouse decidualization. The regulation of estrogen on Abp1 is mediated by transcription factor CCAAT/enhancer-binding protein-β. Abp1 expression is also regulated by cAMP, bone morphogenetic protein 2, and ERK1/2. Abp1 may be essential for mouse embryo implantation and decidualization.

scholarly journals S-nitrosoglutathione inhibits adipogenesis in 3T3-L1 preadipocytes by S-nitrosation of CCAAT/enhancer-binding protein β

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Marion Mussbacher ◽  
Heike Stessel ◽  
Teresa Pirker ◽  
Antonius C. F. Gorren ◽  
Bernd Mayer ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Protein Expression ◽  
Binding Protein ◽  
Total Protein Content ◽  
Fat Cell ◽  
No Donor ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein ◽  
Mrna And Protein Expression ◽  
Adipogenic Effect

Abstract Murine 3T3-L1 adipocytes share many similarities with primary fat cells and represent a reliable in vitro model of adipogenesis. The aim of this study was to probe the effect of S-nitrosoglutathione (GSNO) on adipocyte differentiation. Adipogenesis was induced with a mixture of insulin, dexamethasone, and 3-isobutyl-1-methylxanthine in the absence and presence of increasing GSNO concentrations. Biochemical analysis after 7 days of differentiation showed a prominent anti-adipogenic effect of GSNO which was evident as reduced cellular triglycerides and total protein content as well as decreased mRNA and protein expression of late transcription factors (e.g. peroxisome proliferator activated receptor γ) and markers of terminal differentiation (e.g. leptin). By contrast, the nitrosothiol did not affect mRNA and protein expression of CCAAT/enhancer-binding protein β (C/EBPβ), which represents a pivotal early transcription factor of the adipogenic cascade. Differentiation was also inhibited by the NO donor (Z)-1-[2-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate. Biotin switch experiments showed significantly increased S-nitrosation of C/EBPβ variants indicating that posttranslational S-nitrosative modification of this transcription factor accounts for the observed anti-adipogenic effect of NO. Our results suggest that S-nitrosation might represent an important physiological regulatory mechanism of fat cell maturation.

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