Cross-Regulation of C/EBPα and PPARγ Controls the Transcriptional Pathway of Adipogenesis and Insulin Sensitivity

Wu, Zhidan; Rosen, Evan D.; Brun, Regina P.; Hauser, Stefanie; Adelmant, Guillaume; Troy, Amy E.; McKeon, Catherine; Darlington, Gretchen J.; Spiegelman, Bruce M.

doi:10.1016/s1097-2765(00)80306-8

Cited by 933 publications

(784 citation statements)

References 44 publications

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“…C/EBPa is known to be the downstream target of C/EBPd and C/EBPb, 25 therefore, it can be speculated that the augmentation of expression of the C/EBPa gene might have been due to indirect effects, which were probably caused by the enhanced expression of the C/EBPd gene. In fact, the binding of JDP2 to the C/EBPd and C/EBPb genes was detected but there was no obvious binding to the C/EBPa gene (Figure 6a).…”

Section: Discussionmentioning

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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Section: Discussionmentioning

confidence: 99%

JDP2 suppresses adipocyte differentiation by regulating histone acetylation

Nakade¹,

Pan²,

Yoshiki

et al. 2007

Cell Death Differ

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“…The molecular mechanism(s) that explain(s) how this compound down‐modulates the release of proinflammatory mediators is yet to be deciphered; however, it is known that Rosiglitazone regulates Toll‐like receptor (TLR) signalling in immune cells,146 and controls (increases) the expression of CD36 in innate immune cells146 via cross‐regulation147; therefore, this might provide insights to how Rosiglitazone modulates the proinflammatory responses in immune cells. Interestingly, it was also observed in this clinical trial that the administration of Rosiglitazone led to lower parasite clearance time 145.…”

Section: Taking Advantage Of Immune Regulationmentioning

confidence: 99%

Evaluating antidisease immunity to malaria and implications for vaccine design

Ademolue

Awandare

2017

Immunology

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SummaryImmunity to malaria could be categorized broadly as antiparasite or antidisease immunity. While most vaccine research efforts have focused on antiparasite immunity, the evidence from endemic populations suggest that antidisease immunity is an important component of natural immunity to malaria. The processes that mediate antidisease immunity have, however, attracted little to no attention, and most interests have been directed towards the antibody responses. This review evaluates the evidence for antidisease immunity in endemic areas and discusses the possible mechanisms responsible for it. Given the key role that inflammation plays in the pathogenesis of malaria, regulation of the inflammatory response appears to be a major mechanism for antidisease immunity in naturally exposed individuals.

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“…Of the 24 000 genes examined, we focused on those that contribute to differentiation or development (Table 1). Key genes for the regulation of embryonic organogenesis (Hoxa5, Hoxa9, Foxc1 and Foxf2) and the commitment of immature cells to multiple lineages (Pparg, Cebpa, Plxnd1, Egfl7, Mgp, Plxdc2, Ebf1 and Tcf3) were expressed at higher levels in AO cells than in AX cells, suggesting that AO cells have characteristics of immature mesenchymal cells (Wang and Reed, 1993;Luo et al, 1997;Wu et al, 1999;Rosen et al, 2000;Parker et al, 2004;Torres-Vazquez et al, 2004;Miller et al, 2007;Cole et al, 2008). The profile of AX cells, on the other hand, was indicative of both cells that are committed to the osteocyte lineage (Dlx3, Sp7, Dkk1, Ostn and Bmp3) and cells that are inclined to tumorigenesis in vivo (Cd276, Ptgs2, Vegfa, Epha2, Frzb and Sfrp1) (Kim et al, 1993;Daluiski et al, 2001;Dannenberg et al, 2001;Thomas et al, 2003;Lee et al, 2004 Zang et al, 2007;Brantley-Sieders et al, 2008;Engin et al, 2008;Li et al, 2008).…”

Section: Ao and Ax Cells Differ In Their Gene Expression Profilesmentioning

confidence: 99%

c-MYC overexpression with loss of Ink4a/Arf transforms bone marrow stromal cells into osteosarcoma accompanied by loss of adipogenesis

et al. 2010

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The development of cancer is due to the growth and proliferation of transformed normal cells. Recent evidence suggests that the nature of oncogenic stress and the state of the cell of origin critically affect both tumorigenic activity and tumor histological type. However, this mechanistic relationship in mesenchymal tumors is currently largely unexplored. To clarify these issues, we established a mouse osteosarcoma (OS) model through overexpression of c-MYC in bone marrow stromal cells (BMSCs) derived from Ink4a/Arf (À/À) mice. Single-cell cloning revealed that c-MYC-expressing BMSCs are composed of two distinctly different clones: highly tumorigenic cells, similar to bipotent-committed osteochondral progenitor cells, and low-tumorigenic tripotent cells, similar to mesenchymal stem cells (MSCs). It is noteworthy that both bipotent and tripotent cells were capable of generating histologically similar, lethal OS, suggesting that both committed progenitor cells and MSCs can become OS cells of origin. Shifting mesenchymal differentiation by depleting PPARc in tripotent MSC-like cells and overexpressing PPARc in bipotent cells affected cell proliferation and tumorigenic activity. Our findings indicate that differentiation potential has a key role in OS tumorigenic activity, and that the suppression of adipogenic ability is a critical factor for the development of OS.

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Cross-Regulation of C/EBPα and PPARγ Controls the Transcriptional Pathway of Adipogenesis and Insulin Sensitivity

Cited by 933 publications

References 44 publications

JDP2 suppresses adipocyte differentiation by regulating histone acetylation

JDP2 suppresses adipocyte differentiation by regulating histone acetylation

Evaluating antidisease immunity to malaria and implications for vaccine design

c-MYC overexpression with loss of Ink4a/Arf transforms bone marrow stromal cells into osteosarcoma accompanied by loss of adipogenesis

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