C/EBP-δ Induction by gp130 Signaling

Kamaraju, Anil K.; Adjalley, Sophie H.; Zhang, Peilin; Chebath, Judith; Revel, Michel

doi:10.1074/jbc.m310443200

Cited by 11 publications

(6 citation statements)

References 54 publications

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“…To study the role of LAP to LIP ratio in ER stress-triggered cell death, we used the specific inducers of ER stress tunicamycin (Tm) and thapsigargin (Tg) and murine B16 melanoma clones that inducibly express either LAP or LIP [34]. Clone F10.9-3 constitutively expresses the Tet repressor and carries a vector with a bidirectional inducible promoter encoding wt LAP and GFP.…”

Section: Resultsmentioning

confidence: 99%

“…The murine B16 melanoma clones, F10.9-3 and F10.9-4, were derived from the parental cell line B16-F10 (ATCC CRL-6475) and were kindly provided by M. Revel and J. Chebath (Weizmann Institute of Science) [34]. Human cervical carcinoma HeLa cells (CCL-2.1) and human embryonic kidney cells (HEK 293T) were obtained from the American Type Culture Collection (ATCC), Manassas, VA.…”

Section: Methodsmentioning

confidence: 99%

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C/EBP-β Regulates Endoplasmic Reticulum Stress–Triggered Cell Death in Mouse and Human Models

et al. 2010

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Endoplasmic reticulum (ER) stress elicits the unfolded protein response (UPR), initially aimed at coping with the stress, but triggering cell death upon further stress. ER stress induces the C/EBP-® variant Liver-enriched Activating Protein (LAP), followed by the dominant-negative variant, Liver Inhibitory Protein (LIP). However, the distinct role of LAP and LIP in ER stress is unknown. We found that the kinetics of the ER stress-induced expression of LIP overlapped with that of the cell death in mouse B16 melanoma cells. Furthermore, inducible over-expression of LIP augmented ER stress-triggered cell death whereas over-expression of LAP attenuated cell death. Similar results were obtained in human 293T cells. Limited vasculature in tumors triggers hypoxia, nutrient shortage and accumulation of toxic metabolites, all of which eliciting continuous ER stress. We found that LAP promoted and LIP inhibited B16 melanoma tumor progression without affecting angiogenesis or accelerating the cell cycle. Rather, LAP attenuated, whereas LIP augmented tumor ER stress. We therefore suggest that C/EBP-® regulates the transition from the protective to the death–promoting phase of the UPR. We further suggest that the over-expression of LAP observed in many solid tumors promotes tumor progression by attenuating ER stress–triggered tumor cell death.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

C/EBP-β Regulates Endoplasmic Reticulum Stress–Triggered Cell Death in Mouse and Human Models

et al. 2010

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“…The C/ EBPs are a large family of regulatory factors involved in gene transcription, and knock-down of C/EBPδ was found to inhibit P0 mRNA induced by an interleukin-6 receptor/ ligand (Kamaraju et al 2004), implicating these factors in myelination. In adipocytes, a member of the peroxisome proliferator-activated receptor family, PPARγ, was reduced in the presence of SB203580 (Engelman et al 1998).…”

Section: P38 Mapk Mechanismsmentioning

confidence: 99%

p38 Mitogen-Activated Protein Kinase Regulates Myelination

et al. 2007

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The p38 mitogen-activated protein kinase family is emerging as a crucial signaling molecule for a vast number of cellular functions including cell migration, proliferation, and differentiation. The function of p38 in myelination has only been recently addressed. Using pyridinyl imidazole-based p38 alpha/beta selective inhibitors, we have reported a critical role for this kinase in the regulation of myelination, specifically, in controlling the differentiation of Schwann cells, and oligodendrocytes, the myelinating glia of the peripheral and central nervous systems, respectively. These compounds inhibited the accumulation of myelin-cell-specific markers, including myelin-specific glycosphingolipids, myelin-associated glycoprotein, and myelin basic protein. More significantly, myelination of dorsal root ganglia neurons by oligodendrocytes was irreversibly blocked by p38 inhibitors. Our current studies are focusing on the molecular mechanisms by which p38 regulates oligodendrocyte and Schwann cell differentiation and its role in models of myelination and remyelination.

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“…We have previously shown that cardiac NF-B and AP-1 DNA-binding activity is increased in dTGR. In a positivefeedback loop, gp130/IL-6 signaling induces C/EBP expression (20). HSPs function as molecular chaperones or proteases (8).…”

Section: Discussionmentioning

confidence: 99%

Cardiac gene expression profile in rats with terminal heart failure and cachexia

Wellner

Dechend

Park

et al. 2005

Physiological Genomics

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About one-half of double transgenic rats (dTGR) overexpressing the human renin and angiotensinogen genes die by age 7 wk of terminal heart failure (THF); the other (preterminal) one-half develop cardiac damage but survive. Our study’s aim was to elucidate cardiac gene expression differences in dTGR-THF compared with dTGR showing compensated cardiac hypertrophy but not yet THF. dTGR treated with losartan (LOS) and nontransgenic rats (SD) served as controls. THF-dTGR body weight was significantly lower than for all other groups. At death, THF-dTGR had blood pressures of 228 ± 7 mmHg (cardiac hypertrophy index 6.2 ± 0.1 mg/g). Tissue Doppler showed reduced peak early (Ea) to late (Aa) diastolic expansion in THF-dTGR, indicating diastolic function. Preterminal dTGR had blood pressures of 197 ± 5 mmHg (cardiac hypertrophy index 5.1 ± 0.1 mg/g); Ea < Aa compared with LOS-dTGR (141 ± 6 mmHg; 3.7±0.1 mg/g; Ea > Aa) and SD (112 ± 4 mmHg; 3.6 ± 0.1 mg/g; Ea > Aa). Left ventricular RNA was isolated for the Affymetrix system and TaqMan RT-PCR. THF-dTGR and dTGR showed upregulation of hypertrophy markers and α/β-myosin heavy chain switch to the fetal isoform. THF-dTGR (vs. dTGR) showed upregulation of 239 and downregulation of 150 genes. Various genes of mitochodrial respiratory chain and lipid catabolism were reduced. In addition, genes encoding transcription factors (CEBP-β, c-fos, Fra-1), coagulation, remodeling/repair components (HSP70, HSP27, heme oxygenase), immune system (complement components, IL-6), and metabolic pathway were differentially expressed. In contrast, LOS-dTGR and SD had similar expression profiles. These data demonstrate that THF-dTGR show an altered expression profile compared with preterminal dTGR.

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C/EBP-δ Induction by gp130 Signaling

Cited by 11 publications

References 54 publications

C/EBP-β Regulates Endoplasmic Reticulum Stress–Triggered Cell Death in Mouse and Human Models

C/EBP-β Regulates Endoplasmic Reticulum Stress–Triggered Cell Death in Mouse and Human Models

p38 Mitogen-Activated Protein Kinase Regulates Myelination

Cardiac gene expression profile in rats with terminal heart failure and cachexia

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