Erratum: correction: CREB regulates hepatic gluconeogenesis through the coactivator PGC-1

Herzig, Stephan; Long, Fanxin; Jhala, Ulupi S.; Hedrick, Susan; Quinn, Rebecca; Bauer, Anna; Rudolph, Dorothea; Schütz, Günther; Yoon, Cliff; Puigserver, Pere; Spiegelman, Bruce M.; Montminy, Marc

doi:10.1038/35098123

Cited by 11 publications

(5 citation statements)

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“…For example HIF-1 alpha is known to induce the expression of several genes regulating glycolysis such as hexokinase-2, phosphofructokinase, GAPDH, enolase-1 and LDHA [13]. Approximately 25% of the genes regulated by CREB play a role in the control of metabolic processes [26] and it has been observed that inhibition of CREB induces fastinghyperglycemia and reduces expression of gluconeogenic genes such as phosphoenolpyruvate carboxykinase and glucose-6-phosphatase [43]. Interestingly, it has also been demonstrated that ATF-3 is strongly induced in renal epithelial cells as a result of medium exhaustion [36] suggesting that selective activation of ATF-3 in A459 cells is a consequence of hypoxia induced glucose deprivation.…”

Section: Discussionmentioning

confidence: 99%

Differential Effects of Hypoxic Stress in Alveolar Epithelial Cells and Microvascular Endothelial Cells

Signorelli

Jennings

Leonard

et al. 2010

Cell Physiol Biochem

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Under hypoxic conditions eukaryotic cells and tissues undergo adaptive responses involving glycolysis, angiogenesis, vasoconstriction and inflammation. The underlying molecular mechanisms are not yet fully elucidated and are most likely cell and tissue specific. In the lung, alveolar epithelial cells and microvascular endothelial cells are highly sensitive to hypoxia and together orchestrate a rapid and sustained adaptive response. We examined the effect of different oxygen tensions on cell viability, glucose metabolism, key transcription factors and signaling molecules, in alveolar epithelial cells (A549) and microvascular endothelial cells (HMEC-1). Both cell types tolerated hypoxia without detectable cell injury. Hypoxia induced glycolysis in both epithelial and microvascular endothelial cells, although A549 cells exhibited a higher rate of glucose consumption. The transcription factor CREB (cAMP response element binding protein) was activated with decreasing oxygen tensions in both cell types. This effect was again more marked in A549 cells, demonstrating epithelial cells to be more oxygen sensitive. Activating Transcription Factor 3 (ATF-3) was heavily induced by hypoxia in A549 cells but not in HMEC-1 cells. Both cell types exhibited hypoxia induced secretion of VEGF and IL-6. Secretion of the vasoconstrictor endothelin-1 (ET1) was increased by hypoxia in HMEC-1 cells but decreased in A549 cells. These data reveal that both cell types exhibit an adaptive response to hypoxia but alveolar epithelial cells are generally more sensitive. ET-1 was oppositely regulated by decreased oxygen tensions in the investigated cell types. The present study further elucidates the adaptive molecular mechanisms in pulmonary hypoxia and demonstrates cell specific responses.

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Section: Discussionmentioning

confidence: 99%

Differential Effects of Hypoxic Stress in Alveolar Epithelial Cells and Microvascular Endothelial Cells

Signorelli

Jennings

Leonard

et al. 2010

Cell Physiol Biochem

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“…It is capable of driving transcriptional control of mitochondrial biogenesis through direct interaction with, and coactivation of, PPARs (Madrazo and Kelly, 2008), estrogen-related receptors (ERRs; Schreiber et al, 2004; Eichner and Giguère, 2011), nuclear respiratory factors (NRF-1/NRF-2; Wu et al, 1999; Scarpulla, 2011) and the transcription factor yin-yang one (YY1; Basu et al, 1997; Seelan and Grossman, 1997; Cunningham et al, 2007; Xi et al, 2007), which are important nuclear transcription factors controlling mitochondrial metabolism (Scarpulla et al, 2012). PGC-1 α is also an inducible responder to cellular energetic and metabolic stress, such as cold exposure (Puigserver et al, 1998; Uldry et al, 2006; Fisher et al, 2012), nutrient deprivation (Herzig et al, 2001; Yoon et al, 2001; Handschin et al, 2005; Rhee et al, 2006) and exercise (Baar et al, 2002; Handschin and Spiegelman, 2008) and is dynamically regulated in response to a variety of signaling pathways involved in cellular growth, differentiation and energy metabolism. Additionally, a large amount of evidence suggests that PGC-1 α links mitochondrial biogenesis and the response to oxidative stress.…”

Section: Pgc-1α As a Molecular Target Of Pvi-specific Gxementioning

confidence: 99%

“…It has been reported that methylation of CpG in CRE blocked pCREB binding (Iguchi-Ariga and Schaffner, 1989; Sunahori et al, 2009). CREB is an important regulator for PGC-1 α gene transcription (Herzig et al, 2001; St-Pierre et al, 2006). Barrès et al (2009) provided evidence that PGC-1 α hypermethylation is concomitant with reduced mitochondrial content in type 2 diabetic patients, and links DNMT3B to the acute fatty-acid-induced non-CpG methylation of PGC-1 α promoter.…”

Section: Pgc-1α As a Molecular Target Of Pvi-specific Gxementioning

confidence: 99%

Convergence of genetic and environmental factors on parvalbumin-positive interneurons in schizophrenia

Jiang¹,

Cowell²,

Nakazawa³

2013

Front. Behav. Neurosci.

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Schizophrenia etiology is thought to involve an interaction between genetic and environmental factors during postnatal brain development. However, there is a fundamental gap in our understanding of the molecular mechanisms by which environmental factors interact with genetic susceptibility to trigger symptom onset and disease progression. In this review, we summarize the most recent findings implicating oxidative stress as one mechanism by which environmental insults, especially early life social stress, impact the development of schizophrenia. Based on a review of the literature and the results of our own animal model, we suggest that environmental stressors such as social isolation render parvalbumin-positive interneurons (PVIs) vulnerable to oxidative stress. We previously reported that social isolation stress exacerbates many of the schizophrenia-like phenotypes seen in a conditional genetic mouse model in which NMDA receptors (NMDARs) are selectively ablated in half of cortical and hippocampal interneurons during early postnatal development (Belforte et al., 2010). We have since revealed that this social isolation-induced effect is caused by impairments in the antioxidant defense capacity in the PVIs in which NMDARs are ablated. We propose that this effect is mediated by the down-regulation of PGC-1α, a master regulator of mitochondrial energy metabolism and anti-oxidant defense, following the deletion of NMDARs (Jiang et al., 2013). Other potential molecular mechanisms underlying redox dysfunction upon gene and environmental interaction will be discussed, with a focus on the unique properties of PVIs.

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“…PGC-1α mRNA levels are elevated in the liver of rodents in models of type 2 diabetes; this is likely due to alterations of hepatic insulin resistance. 38,39 Acute knockdown of PGC-1α in the liver improves hepatic insulin sensitivity and glucose tolerance in db/db mice. 40 Thus modulating PGC-1α activity in the liver may have important implications for systemic glucose homeostasis.…”

Section: Bfementioning

confidence: 99%

Effects of flavonoid-rich Chinese bayberry (Morella rubra Sieb. et Zucc.) fruit extract on regulating glucose and lipid metabolism in diabetic KK-A^ymice

Zhang

Jia

et al. 2016

Food Funct.

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In the present study, male diabetic KK-A(y) mice were used to investigate the antidiabetic effect of bayberry fruit extract (BFE, 200 mg kg(-1)) by gavage for 5 weeks. BFE significantly lowered fasting blood glucose, improved glucose tolerance and insulin sensitivity in KK-A(y) mice. It significantly reduced serum concentrations of glucose, lipids, inflammation, and liver function markers, including insulin, glucagon, leptin, total cholesterol, triglycerides, low density lipoprotein, interleukin-1β, and alanine transferase in KK-A(y) mice. Liver weight and liver lipid accumulation were also markedly reduced by BFE in mice. The hypoglycemic effect of BFE appeared to be partially mediated through the inhibition of hepatic gluconeogenesis, which was supported by the reduced PPARγ coactivator 1-alpha (PGC-1α) and phosphoenolpyruvate carboxykinase (PEPCK) mRNA expressions in the liver of KK-A(y) mice and by the decreased glucose production, increased glycolysis as well as the reduced gene expression levels of PGC-1α, PEPCK, and glucose-6-phosphatase (G6Pase) in HepG2 cells. Gene expressions of hepatic lipid metabolism and inflammatory markers were also down-regulated by BFE in the liver of KK-A(y) mice. Furthermore, BFE promoted hepatic phosphorylation of AMPKα (Thr172) both in vivo and in vitro. Therefore, the activation of the AMPK pathway may play an important role in the antidiabetic effects of BFE, and red Chinese bayberry fruits may be an effective dietary food for the management of type 2 diabetes and its complications.

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Erratum: correction: CREB regulates hepatic gluconeogenesis through the coactivator PGC-1

Cited by 11 publications

References 1 publication

Differential Effects of Hypoxic Stress in Alveolar Epithelial Cells and Microvascular Endothelial Cells

Differential Effects of Hypoxic Stress in Alveolar Epithelial Cells and Microvascular Endothelial Cells

Convergence of genetic and environmental factors on parvalbumin-positive interneurons in schizophrenia

Effects of flavonoid-rich Chinese bayberry (Morella rubra Sieb. et Zucc.) fruit extract on regulating glucose and lipid metabolism in diabetic KK-A^ymice

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Erratum: correction: CREB regulates hepatic gluconeogenesis through the coactivator PGC-1

Cited by 11 publications

References 1 publication

Differential Effects of Hypoxic Stress in Alveolar Epithelial Cells and Microvascular Endothelial Cells

Differential Effects of Hypoxic Stress in Alveolar Epithelial Cells and Microvascular Endothelial Cells

Convergence of genetic and environmental factors on parvalbumin-positive interneurons in schizophrenia

Effects of flavonoid-rich Chinese bayberry (Morella rubra Sieb. et Zucc.) fruit extract on regulating glucose and lipid metabolism in diabetic KK-Aymice

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Product

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Effects of flavonoid-rich Chinese bayberry (Morella rubra Sieb. et Zucc.) fruit extract on regulating glucose and lipid metabolism in diabetic KK-A^ymice