Conditional ectopic expression of C/EBP beta in NIH-3T3 cells induces PPAR gamma and stimulates adipogenesis.

Wu, Zhidan; Xie, Yanjun; Bucher, Nancy L. R.; Farmer, Stephen R.

doi:10.1101/gad.9.19.2350

Cited by 496 publications

(382 citation statements)

References 42 publications

(58 reference statements)

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“…Indeed, under circumstances when PPAR␥ is already expressed, RA can lead to the loss of expression of PPAR␥, consistent with its ability to block the transcriptional activity of C/EBP␤, which induces PPAR␥ during adipogenesis (12,23). To further the use of RA as a tool for understanding the stages of adipocyte differentiation, we first tested the ability of RA to affect the adipogenesis of 3T3-L1 cells that is induced by the PPAR␥2 activator, BRL49653.…”

Section: Ra Inhibits Ppar␥ Ligand-mediated Adipogenesis In 3t3 L1mentioning

confidence: 99%

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Peroxisome Proliferator Activated Receptor γ, CCAAT/ Enhancer-binding Protein α, and Cell Cycle Status Regulate the Commitment to Adipocyte Differentiation

Shao

Lazar

1997

Journal of Biological Chemistry

259

174

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Terminal differentiation of stem cells is characterized by cessation of cell proliferation as well as changes in cell morphology associated with the differentiated state. For adipocyte differentiation, independent lines of evidence show that the transcription factors peroxisome proliferator activated receptor ␥ (PPAR␥) and CCAAT/ enhancer-binding protein ␣ (C/EBP␣) as well as the tumor suppressor retinoblastoma (Rb) protein are essential. How these proteins promote adipocyte conversion and how they function cooperatively during the differentiation process remain unclear. We have used retinoic acid (RA) inhibition of adipogenesis to investigate these issues. RA blocked adipogenesis of 3T3-L1 cells induced to differentiate by ectopic expression of PPAR␥ and C/EBP␣ independently or together. However, under these circumstances RA was only effective at preventing adipogenesis when added prior to confluence, suggesting that factors involved in regulation of the cell cycle might play a role in establishing the commitment state of adipogenesis that is insensitive to RA. During differentiation of wild type 3T3 L1 preadipocytes, we found that Rb protein is hyperphosphorylated early in adipogenesis, corresponding to previously quiescent cells reentering the cell cycle, and later becomes hypophosphorylated. The data suggest that, together with the coexpression of PPAR␥ and C/EBP␣, permanent exit from the cell cycle establishes the irreversible commitment to adipocyte differentiation.

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Section: Ra Inhibits Ppar␥ Ligand-mediated Adipogenesis In 3t3 L1mentioning

confidence: 99%

“…7). Enforced expression of PPAR␥ (8), C/EBP␣ (9 -11), or C/EBP␤ (10,12,13) stimulates adipogenesis in NIH 3T3 fibroblasts, suggesting the essential roles of these transcription factors in regulating adipogenesis. Furthermore, combined expression of PPAR␥ and C/EBP␣ has synergistic effects on promoting fat cell conversion in myoblasts (14).…”

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confidence: 99%

Peroxisome Proliferator Activated Receptor γ, CCAAT/ Enhancer-binding Protein α, and Cell Cycle Status Regulate the Commitment to Adipocyte Differentiation

Shao

Lazar

1997

Journal of Biological Chemistry

259

174

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“…4 These transcription factors bind to specific sequences in the promoters of the C/EBPa gene and the PPARg2 gene, inducing their expression, which, in turn, activates the full adipogenic program of gene expression. [8][9][10] Expression of PPARg2 is also induced via an SREBP-1c-dependent pathway. 11 Once PPARg2 and C/EBPa have been activated, 'cross-talk' between PPARg2 and C/EBPa maintains the expression of each protein during adipocyte differentiation, even in the absence of C/EBPb and C/EBPd.…”

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confidence: 99%

JDP2 suppresses adipocyte differentiation by regulating histone acetylation

Nakade¹,

Pan²,

Yoshiki

et al. 2007

Cell Death Differ

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Among the events that control cellular differentiation, the acetylation of histones plays a critical role in the regulation of transcription and the modification of chromatin. Jun dimerization protein 2 (JDP2), a member of the AP-1 family, is an inhibitor of such acetylation and contributes to the maintenance of chromatin structure. In an examination of Jdp2 'knock-out' (KO) mice, we observed elevated numbers of white adipocytes and significant accumulation of lipid in the adipose tissue in sections of scapulae. In addition, mouse embryo fibroblasts (MEFs) from Jdp2 KO mice were more susceptible to adipocyte differentiation in response to hormonal induction and members of the CCAAT/enhancer-binding proteins (C/EBP) gene family were expressed at levels higher than MEFs from wild-type mice. Furthermore, JDP2 inhibited both the acetylation of histone H3 in the promoter of the gene for C/EBPd and transcription from this promoter. Our data indicate that JDP2 plays a key role as a repressor of adipocyte differentiation by regulating the expression of the gene for C/EBPd via inhibition of histone acetylation.

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“…Some studies have demonstrated that overexpression of C/EBPb in NIH3T3 cells can induce adipogenesis in the presence of adipogenic inducers [45]. Expression of C/ EBPb in NIH3T3 cells activates the synthesis of PPARg mRNA that stimulates their conversion into adipocytes [46]. It has been shown that MAPK initiates the activation of C/EBPb by phosphorylation [47,48], suggesting that MAPK could be involved in adipocyte differentiation.…”

Section: Discussionmentioning

confidence: 99%

Increased mitogen-activated protein kinase expression and activity in white adipose tissue of ventromedial hypothalamus-lesioned rats

et al. 1997

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In rats made obese by electrolytic lesion of the ventromedial hypothalamus (VMH), the onset of the syndrome is determined by the time of the lesion, allowing a chronological study of the alterations associated with obesity. Lesion of the VMH induces hyperphagia, hyperinsulinaemia and obesity [1], associated with alterations in the cellularity and metabolism of the white adipose tissue (WAT). After the lesion, there is an initial period of rapid weight gain (dynamic phase) followed by a slowing in the rate of weight gain (static phase). During the dynamic phase of the VMH obesity, a state of hyperresponsiveness to insulin is observed in white adipose tissue [2]. This Diabetologia (1997) 40: 533-540 Increased mitogen-activated protein kinase expression and activity in white adipose tissue of ventromedial hypothalamus-lesioned rats Summary Ventromedial hypothalamus lesions in rats induce hyperphagia and hyperinsulinaemia associated with a rapid growth of white adipose tissue resulting in massive obesity. It has been shown previously that at an early stage after the lesion, during the dynamic phase of obesity, the white adipose tissue is hyper-responsive to insulin. In the present work, we show that the effects of insulin on the autophosphorylation of the insulin receptor and on its tyrosine-kinase activity towards endogenous substrates are similar in intact adipocytes of control and ventromedial hypothalamus lesioned rats. One week after the lesion, the expression of phosphatidylinisitol 3-kinase and RAF-1 kinase, evaluated by Western-blotting, was similar in control and ventromedial hypothalamus lesioned rats. In contrast, an important increase in the expression of extracellular signal regulated kinase 1 protein was observed in white adipose tissue of ventromedial hypothalamus lesioned compared to control animals. No difference in the expression of extracellular signal regulated kinase 1 mRNA was observed in adipose tissue of control and ventromedial hypothalamus lesioned rats, suggesting that a posttranscriptional mechanism is involved in the over-expression of extracellular signal regulated kinase 1. The kinase activity of extracellular signal regulated kinase 1 and 2 is also markedly increased in adipocytes of ventromedial hypothalamus lesioned compared to control rats, both in the basal state and after insulin stimulation. Six weeks after the ventromedial hypothalamus lesion, this increase in mitogen-activated protein kinase expression and activity was still observed in adipocytes of ventromedial hypothalamus lesioned rats. These results suggest that an early and sustained increase in the expression and activity of mitogen-activated protein kinase may participate in the development of white adipose tissue in ventromedial hypothalamus lesioned rats. [Diabetologia (1997) 40: 533-540]

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Conditional ectopic expression of C/EBP beta in NIH-3T3 cells induces PPAR gamma and stimulates adipogenesis.

Cited by 496 publications

References 42 publications

Peroxisome Proliferator Activated Receptor γ, CCAAT/ Enhancer-binding Protein α, and Cell Cycle Status Regulate the Commitment to Adipocyte Differentiation

Peroxisome Proliferator Activated Receptor γ, CCAAT/ Enhancer-binding Protein α, and Cell Cycle Status Regulate the Commitment to Adipocyte Differentiation

JDP2 suppresses adipocyte differentiation by regulating histone acetylation

Increased mitogen-activated protein kinase expression and activity in white adipose tissue of ventromedial hypothalamus-lesioned rats

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