scholarly journals Cyclic AMP-induced Forkhead Transcription Factor, FKHR, Cooperates with CCAAT/Enhancer-binding Protein β in Differentiating Human Endometrial Stromal Cells

2002 ◽  
Vol 277 (23) ◽  
pp. 20825-20832 ◽  
Author(s):  
Mark Christian ◽  
Xiaohui Zhang ◽  
Tanja Schneider-Merck ◽  
Terry G. Unterman ◽  
Birgit Gellersen ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cyclic Amp ◽  
Stromal Cells ◽  
Binding Protein ◽  
Forkhead Transcription Factor ◽  
Endometrial Stromal Cells ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein

scholarly journals Transcription Factor CCAAT Enhancer-binding Protein β (C/EBPβ) Regulates the Formation of a Unique Extracellular Matrix That Controls Uterine Stromal Differentiation and Embryo Implantation

2011 ◽  
Vol 286 (22) ◽  
pp. 19860-19871 ◽  
Author(s):  
Cyril Ramathal ◽  
Wei Wang ◽  
Elizabeth Hunt ◽  
Indrani C. Bagchi ◽  
Milan K. Bagchi
Keyword(s):  
Extracellular Matrix ◽  
Transcription Factor ◽  
Basal Lamina ◽  
Stromal Cells ◽  
Binding Protein ◽  
Embryo Implantation ◽  
Major Constituent ◽  
Enhancer Binding Protein ◽  
Decidual Cells ◽  
Ccaat Enhancer Binding Protein

During implantation, the uterine stromal cells undergo terminal differentiation into decidual cells, which support the proper progression of maternal-embryo interactions to successful establishment of pregnancy. The decidual cells synthesize extracellular matrix (ECM) components, such as laminins and collagens, which assemble into a unique basal lamina-like network that surrounds these cells. The functional significance of this matrix during implantation is unknown. We previously showed that the transcription factor CCAAT enhancer-binding protein β (C/EBPβ) critically regulates decidualization in the mouse. We now provide evidence that C/EBPβ directly controls the Lamc1 gene, which encodes a predominant laminin constituent of the ECM produced by the decidual cells. Suppression of Lamc1 expression in mouse primary endometrial stromal cells prevented the assembly of this ECM and impaired stromal differentiation. Attenuation of expression of integrin β1, a major constituent of the integrin receptors targeted by decidual laminins, also inhibited this differentiation process. Disruption of laminin-integrin interactions led to impaired activation of the focal adhesion kinase, an integrin-mediated regulator of cytoskeletal remodeling during decidualization. To further analyze the role of the decidual ECM in modulating maternal-embryo interactions, we monitored trophoblast invasion into differentiating uterine stromal monolayers, using a co-culture system. Silencing of stromal Lamc1 expression, which prevented formation of the basal lamina-like matrix, resulted in marked reduction in trophoblast outgrowth. Collectively, our findings identified C/EBPβ as a critical regulator of the unique ECM that controls decidual cell architecture and differentiation, and it provided new insights into the mechanisms by which the uterine stromal microenvironment controls the progression of embryo implantation.

The role of the CCAAT/enhancer-binding protein in the transcriptional regulation of the gene for phosphoenolpyruvate carboxykinase (GTP)

1990 ◽  
Vol 10 (12) ◽  
pp. 6264-6272
Author(s):  
E A Park ◽  
W J Roesler ◽  
J Liu ◽  
D J Klemm ◽  
A L Gurney ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Binding Protein ◽  
Regulatory Elements ◽  
Specific Protein ◽  
Affinity Column ◽  
Binding Domains ◽  
Nuclear Extracts ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein

Previous studies have identified a region in the promoter of the gene for phosphoenolpyruvate carboxykinase (GTP) (PEPCK) (positions -460 to +73) containing the regulatory elements which respond to cyclic AMP, glucocorticoids, and insulin and confer the tissue- and developmental stage-specific properties to the gene. We report that CCAAT/enhancer-binding protein (C/EBP) binds to the cyclic AMP-responsive element CRE-1 as well as to two regions which have been previously shown to bind proteins enriched in liver nuclei. The DNase I footprint pattern provided by the recombinant C/EBP was identical to that produced by a 43-kDa protein purified from rat liver nuclear extracts, using a CRE oligonucleotide affinity column, which was originally thought to be the CRE-binding protein CREB. Transient contransfection experiments using a C/EBP expression vector demonstrated that C/EBP could trans activate the PEPCK promoter. The trans activation occurred through both the upstream, liver-specific protein-binding domains and the CRE. The CRE-binding protein bound only to CRE-1 and not to the upstream C/EBP-binding sites. The results of this study, along with physiological properties of C/EBP, indicate an important role for this transcription factor in providing the PEPCK gene with several of its regulatory characteristics.

Role of transcription factor CCAAT/enhancer-binding protein alpha in human fetal liver cell typesin vitro

2014 ◽  
Vol 45 (8) ◽  
pp. 919-932 ◽  
Author(s):  
Jörg C. Gerlach ◽  
Patrick Over ◽  
Hubert G. Foka ◽  
Morris E. Turner ◽  
Robert L. Thompson ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Liver Cell ◽  
Fetal Liver ◽  
Binding Protein ◽  
Human Fetal Liver ◽  
Fetal Liver Cell ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein

Overexpression of CCAAT Enhancer-Binding Protein α Inhibits the Growth of K562 Cells via the Foxo3a-Bim Pathway

2016 ◽  
Vol 136 (2) ◽  
pp. 65-70 ◽  
Author(s):  
Guili Zhang ◽  
Fei Dong ◽  
Caifu Luan ◽  
Xia Zhang ◽  
Huiyuan Shao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Binding Protein ◽  
K562 Cells ◽  
Cell Counting ◽  
Stable Cell Line ◽  
Mrna Levels ◽  
Forkhead Transcription Factor ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein ◽  
Blood Specimens

We aimed to investigate the role of CCAAT enhancer-binding protein α (C/EBPα) in the pathogenesis of chronic myeloid leukemia (CML) and the mechanism underlying its effect. Bone marrow specimens from 50 patients with CML and peripheral blood specimens from 20 healthy individuals were collected. K562 cells were treated with imatinib. Subsequently, a stable cell line, K562-C/EBPα, was constructed. Cell proliferation was assayed with cell counting kit-8, and mRNA levels of C/EBPα, forkhead transcription factor FKHRL1 (Foxo3a) and Bim were detected by semiquantitative PCR. The correlation of C/EBPα and BCR-ABL was assessed by Spearman's correlation analysis. The results showed that C/EBPα mRNA levels were significantly reduced in CML patients compared with healthy subjects (p < 0.001) and were negatively correlated with BCR-ABL1 (r = -0.5046, p < 0.01). Additionally, imatinib enhanced the expression of C/EBPα in K562 cells compared with untreated cells (p < 0.05). Overexpression of C/EBPα significantly decreased cell proliferation and upregulated the expressions of the apoptosis-related genes Foxo3a (p < 0.01) and Bim (p < 0.05) in K562 cells. In conclusion, C/EBPα expression was decreased in patients with CML. Imatinib enhances the expression of C/EBPα in K562 cells, and the overexpression of C/EBPα inhibits cell proliferation and increases apoptosis via the Foxo3a-Bim pathway.

scholarly journals A CCAAT/Enhancer Binding Protein β Isoform, Liver-Enriched Inhibitory Protein, Regulates Commitment of Osteoblasts and Adipocytes

2005 ◽  
Vol 25 (5) ◽  
pp. 1971-1979 ◽  
Author(s):  
Kenji Hata ◽  
Riko Nishimura ◽  
Mio Ueda ◽  
Fumiyo Ikeda ◽  
Takuma Matsubara ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Osteoblast Differentiation ◽  
Molecular Mechanisms ◽  
Binding Protein ◽  
Mesenchymal Cells ◽  
Dominant Negative ◽  
Inhibitory Protein ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein

ABSTRACT Although both osteoblasts and adipocytes have a common origin, i.e., mesenchymal cells, the molecular mechanisms that define the direction of two different lineages are presently unknown. In this study, we investigated the role of a transcription factor, CCAAT/enhancer binding protein β (C/EBPβ), and its isoform in the regulation of balance between osteoblast and adipocyte differentiation. We found that C/EBPβ, which is induced along with osteoblast differentiation, promotes the differentiation of mesenchymal cells into an osteoblast lineage in cooperation with Runx2, an essential transcription factor for osteogenesis. Surprisingly, an isoform of C/EBPβ, liver-enriched inhibitory protein (LIP), which lacks the transcriptional activation domain, stimulates transcriptional activity and the osteogenic action of Runx2, although LIP inhibits adipogenesis in a dominant-negative fashion. Furthermore, LIP physically associates with Runx2 and binds to the C/EBP binding element present in the osteocalcin gene promoter. These data indicate that LIP functions as a coactivator for Runx2 and preferentially promotes the osteoblast differentiation of mesenchymal cells. Thus, identification of a novel role of the C/EBPβ isoform provides insight into the molecular basis of the regulation of osteoblast and adipocyte commitment.

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