FOXO3A Regulates Peroxiredoxin III Expression in Human Cardiac Fibroblasts

Chiribau, Calin B.; Cheng, Lihong; Cucoranu, Ioan; Yu, Yonghao; Clempus, Roza E.; Sorescu, Dan C.

doi:10.1074/jbc.m710610200

Cited by 128 publications

(101 citation statements)

References 26 publications

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“…However, the Prdx3 promoter activity was higher when the full-length Prdx3 versus the partial Prdx3 promoter was transfected in U-937. These results indicate that other Prdx3-c-MYC binding sites 20 and other transcription factors are essentials for Prdx3 transcription, as recently demonstrated by Chiribau et al 48 Further evidence that c-MYC regulates the expression of many genes involved in mitochondrial function 49 and that in other cell systems downregulation of c-MYC promotes apoptosis through the activation of the mitochondrial pathway 49 supports our findings.…”

Section: Discussionsupporting

confidence: 78%

Downregulation of the c‐MYC target gene, peroxiredoxin III, contributes to arsenic trioxide‐induced apoptosis in acute promyelocytic leukemia

Vivas‐Mejía

Özpolat

Chen³

et al. 2009

Intl Journal of Cancer

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Arsenic trioxide (ATO) induces differentiation and apoptosis in acute promyelocytic leukemia (APL). Several reports indicate that in APL cells apoptosis occurs mainly by a mechanism that involves the inhibition of glutathione peroxidase, one of the enzymes that regulates mitochondrial levels of H 2 O 2 . Peroxiredoxin (Prx) III, a c-MYC target gene, is also a mitochondria-specific H 2 O 2 -scavenger enzyme. We studied here the role of Prx III during ATO-induced apoptosis in APL-derived NB4 cells, since these cells express high levels of Prx III. The protein and mRNA levels of Prx III decreased during ATO-induced apoptosis of NB4 cells. The downregulation of Prx III occurred before reactive oxygen species accumulation, reduction in the mitochondrial membrane potential and apoptosis. Depletion of Prx III enhanced mitochondrial-dependent apoptosis events. In contrast, overexpression of Prx III led to reduced levels of ATO-induced apoptosis. c-MYC was also downregulated in ATO-treated NB4 cells. Furthermore, depletion of c-MYC also reduced the Prx-III expression levels. Finally chromatin immunoprecipitation and luciferase reporter assays confirmed that downregulation of Prx-III was caused by the reduction of c-MYC levels during ATO-induced apoptosis of NB4 cells. These findings demonstrate a novel apoptotic-response pathway whereby downregulation of Prx-III potentiates ATO-induced apoptosis in APL cells. ' 2009 UICC

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Section: Discussionsupporting

confidence: 78%

Downregulation of the c‐MYC target gene, peroxiredoxin III, contributes to arsenic trioxide‐induced apoptosis in acute promyelocytic leukemia

Vivas‐Mejía

Özpolat

Chen³

et al. 2009

Intl Journal of Cancer

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“…30 Briefly, complementary single-stranded oligonucleotides were annealed, and the resultant doublestranded DNA fragments were labeled with [␥-32 P]ATP using T4 Polynucleotide Kinase (NEB, Beverly, MA). 32 Plabeled and unlabeled double-stranded oligonucleotides were used as the probe and cold probe, respectively.…”

Section: Nuclear Extract Preparation and Electrophoretic Mobility Shimentioning

confidence: 99%

GGPPS, a New EGR-1 Target Gene, Reactivates ERK 1/2 Signaling through Increasing Ras Prenylation

Shen

Shao

Lai

et al. 2011

The American Journal of Pathology

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Cigarette smoke activates the extracellular signal-regulated kinase (ERK) 1/2 mitogen activated-protein kinase pathway, which, in turn, is responsible for early growth response gene-1 (EGR-1) activation. Here we provide evidence that EGR-1 activation can also reactivate ERK 1/2 mitogen activated-protein kinase through a positive feedback loop through its target gene (geranylgeranyl diphosphate synthase) GGPPS. For the first time, the GGPPS gene is identified as a target of EGR-1, as EGR-1 can directly bind to the predicted consensus-binding site in the GGPPS promoter and regulate its transcription. Long-term observations show that there are two ERK 1/2 phosphorylation peaks after cigarette smoke extract stimulation in human lung epithelial Beas-2B cells. The first peak (at 10 minutes) is responsible for EGR-1 accumulation, and the second (at 4 hours) is diminished after the disruption of EGR-1 transcriptional activity. EGR-1 overexpression enhances Ras prenylation and membrane association in a GGPPS-dependent manner, and it augments ERK 1/2 activation. Likewise, a great reduction of the second peak of ERK 1/2 phosphorylation is observed during long-term cigarette smoke extract stimulation in cells where GGPPS is disrupted. Thus, we have uncovered an intricate positive feedback loop in which ERK 1/2-activated EGR-1 promotes ERK 1/2 reactivation through promoting GGPPS transcription, which might affect cigarette smoke-related lung pathological processes.

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“…Quantification of mouse ␣-SMA, plasminogen activator inhibitorϪ1 (PAI-1), and collagen 1A1 and 18S rRNA was performed by amplification of cDNA using the LightCycler real-time thermocycler as described previously. 32,33 Optimized amplification conditions were 100 nmol/L primers for murine PAI-1, Collagen 1A1 and ␣SMA, 4 mmol/L MgCl 2 , annealing at 68°C; for 18S, 50 nmol/L universal 18S rRNA primers, 4 mmol/L MgCl 2 and annealing at 62°C; extension at 72°C. Copy numbers were calculated by the instrument software from standard curves generated from human PAI-1, Collagen 1A1, ␣SMA and 18S templates.…”

Section: Quantitative Pcrmentioning

confidence: 99%

Inhibition of NF-κB Signaling Reduces Virus Load and Gammaherpesvirus-Induced Pulmonary Fibrosis

Krug

Torres-González

Qin

et al. 2010

The American Journal of Pathology

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Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disorder of unknown etiology. Several studies have demonstrated an association between pulmonary infection with a herpesvirus and IPF. Based on those observations, we have developed a mouse model in which interferon (IFN)␥R؊/؊ mice infected intranasally with murine gammaherpesvirus 68 (MHV68) develop lung fibrosis. We hypothesize that viral load was a critical factor for the development of fibrosis. Because nuclear factor (NF)-B signaling is required to efficiently establish gammaherpesvirus, latency we infected IFN␥R Idiopathic pulmonary fibrosis (IPF) is a destructive lung disease of unknown cause, with no proven effective therapy other than lung transplantation.1 Although the cellular and molecular pathways that drive the pathogenesis of IPF are complex and not fully delineated, increasing evidence suggests that a key event in its pathogenesis is ongoing alveolar epithelial injury in association with an abnormal host repair response. Several studies have implicated viral infections as an important factor in IPF pathogenesis. Specifically, Epstein-Barr virus (EBV) DNA and protein have been detected in 40 to 70% of lung tissue of IPF patients, compared with 10 to 17% of lung controls.2-7 Our group has detected viral DNA for EBV, Kaposi's sarcoma-associated herpesvirus (KSHV), and Cytomegalovirus herpesvirus in Ͼ95% of lung samples of IPF patients, with statically higher frequency compared with patients with non-IPF lung diseases. 5 We have developed a model of chronic herpesvirusinduced pulmonary fibrosis infection using the herpesvirus murine gammaherpesvirus 68 (MHV68), a natural pathogen of wild murid rodents that has strong genetic and biological similarities with the human gammaherpesviruses EBV and KSHV. 8 -10 In immunocompetent animals, intranasal infection with MHV68 leads to an acute phase of lytic replication in the lung. Within several weeks, infectious virus is undetectable, and latent virus

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FOXO3A Regulates Peroxiredoxin III Expression in Human Cardiac Fibroblasts

Cited by 128 publications

References 26 publications

Downregulation of the c‐MYC target gene, peroxiredoxin III, contributes to arsenic trioxide‐induced apoptosis in acute promyelocytic leukemia

Downregulation of the c‐MYC target gene, peroxiredoxin III, contributes to arsenic trioxide‐induced apoptosis in acute promyelocytic leukemia

GGPPS, a New EGR-1 Target Gene, Reactivates ERK 1/2 Signaling through Increasing Ras Prenylation

Inhibition of NF-κB Signaling Reduces Virus Load and Gammaherpesvirus-Induced Pulmonary Fibrosis

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