Investigating transcriptional regulation of Prdx6 in mouse liver cells

Gallagher, Bridget; Phelan, Shelley A.

doi:10.1016/j.freeradbiomed.2007.01.023

Cited by 56 publications

(45 citation statements)

References 41 publications

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“…As a result of these functions, Prdx6 appears to be involved in phospholipid metabolism and membrane turnover Manevich and Fisher, 2005), and we and others have demonstrated that Prdx6 protects cells from ROS-mediated membrane damage and apoptosis Pak et al, 2002;Phelan et al, 2003;Wang et al, 2003;Wang et al, 2004;. Prior studies from our lab have reported an abundance of Prdx6 in liver (Sparling and Phelan, 2003;Wang et al, 2003), and its transcriptional regulation by various oxidative stresses in H2.35 cells, a virally transformed mouse hepatocyte cell line (Sparling and Phelan, 2003;Simeone and Phelan, 2005;Gallagher and Phelan, 2007). A recent report demonstrated that Prdx6-knockout mice exhibit a significant increase in hepatocellular injury (Eismann et al, 2009), confirming an important antioxidant role for this protein in liver.…”

Section: Introductionmentioning

confidence: 85%

“…Various deletions of the Prdx6 mouse promoter had previously been cloned into the pSEAP2-Basic vector (Clontech) by our laboratory, as previously described (Gallagher and Phelan, 2007). These included constructs containing the mouse Prdx6 promoter fragment that extends to nucleotide position -184 (relative to the +1 transcription start site).…”

Section: Synthesis Of Deletion Constructs and Transfectionsmentioning

confidence: 99%

“…We previously determined that Prdx6 expression is significantly inhibited in H2.35 cells upon serum deprivation (Gallagher and Phelan, 2007). To quantify this effect and compare this response to that of Prdx1, we examined the expression of both genes in the presence and absence of serum.…”

Section: Induction Of Prdx1 and Prdx6 Mrna By Serum And Tpamentioning

confidence: 99%

“…We previously synthesized several deletion constructs of the mouse Prdx6 promoter, linked to the pSEAP2-basic reporter gene (Gallagher and Phelan, 2007). We analyzed the smallest of these fragments, containing the proximal 184 nucleotides of the mouse Prdx6 promoter, for consensus transcription factor binding sites against the TransFac4.0 database (Heinemeyer et al, 1998).…”

Section: Identification Of Sp1 Sites In Prdx6 Promotermentioning

confidence: 99%

“…Prdx1 mRNA is upregulated by hypoxia, H 2 0 2 , and tert-BOOH (Prosperi et al, 1998;Li et al, 2002;Rhee et al, 2005;Kim et al, 2007), as well as serum (Prosperi et al, 1998). Likewise, Prdx6 expression is induced by hyperoxia, H 2 0 2 , and nitric oxide Kim et al, 2003;Sparling and Phelan, 2003;Simeone and Phelan, 2005;Chowdhury et al, 2007;Diet et al, 2007;Gallagher and Phelan, 2007;Chowdhury et al, 2009), and also by growth stimuli including keratinocyte growth factor (KGF) Munz et al, 1997;Sparling and Phelan, 2003;Gallagher and Phelan, 2007), lens epithelium-derived growth factor (LEDGF) (Fatma et al, 2001), and TNF- (Kubo et al, 2006;Gallagher and Phelan, 2007). One of the most significant differences we observed between Prdx1 and Prdx6 in the present study is their expression in growing vs. quiescent cells.…”

Section: Regulation Of Peroxiredoxins By Serummentioning

confidence: 99%

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Induction of Prdx1 and Prdx6 in Liver Cells by Serum and TPA

Gardiner¹,

Gaynor²,

Phelan³

2010

IJB

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Peroxiredoxins are thiol-specific antioxidants that protect cells from oxidative damage and have proliferative and anti-apoptotic activity. We investigated the effect of serum and phorbol ester treatment on expression of Prdx1 and Prdx6 in H2.35 cells, and the possible role of Sp1 on Prdx6 induction. Serum stimulation induced a 30% increase in Prdx1 mRNA and a three-fold increase in Prdx6 mRNA. We showed a similar effect of phorbol ester treatment, which led to a 30% increase in Prdx1 mRNA, and over a two-fold increase in Prdx6 expression. Analysis of the Prdx6 proximal promoter sequence revealed four consensus Sp1 sites. Inhibition of Sp1 with mithramycin A blocked Prdx6 induction by TPA and inhibited the serum-induced transcriptional activity of the Prdx6 proximal promoter. These data suggest an important role for Prdx6 in the cellular response to serum and TPA, and implicate Sp1 as a possible mediator of Prdx6 regulation.

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Section: Introductionmentioning

confidence: 85%

Section: Synthesis Of Deletion Constructs and Transfectionsmentioning

confidence: 99%

Section: Induction Of Prdx1 and Prdx6 Mrna By Serum And Tpamentioning

confidence: 99%

Section: Identification Of Sp1 Sites In Prdx6 Promotermentioning

confidence: 99%

Section: Regulation Of Peroxiredoxins By Serummentioning

confidence: 99%

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Induction of Prdx1 and Prdx6 in Liver Cells by Serum and TPA

Gardiner¹,

Gaynor²,

Phelan³

2010

IJB

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Structure and Function of the Human Peroxiredoxin‐Based Antioxidant System: the Interplay between Peroxiredoxins, Thioredoxins, Thioredoxin Reductases, Sulfiredoxins and Sestrins

Szabó

Line

Eggleton

et al. 2009

Redox Signaling and Regulation in Biology and Medicine

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The phospholipase A2 activity of peroxiredoxin 6 promotes cancer cell death induced by tumor necrosis factor alpha in hepatocellular carcinoma

Zhuang

et al. 2015

Mol. Carcinog.

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In this study, we used proteomic profiling to compare hepatocellular carcinoma (HCC) and peri-tumoral tissues to identify potential tumor markers of HCC. We identified eight differentially expressed proteins (>3-fold), including Peroxiredoxin 6 (PRDX6). PRDX6 is a bifunctional enzyme with both peroxidase and calcium-independent phospholipase A2 (iPLA2) activity. We found that peri-tumoral tissues expressed higher levels of PRDX6 mRNA (n = 59, P = 0.018) and protein (n = 265, P < 0.001) than HCC tissues, and that decreased expression of PRDX6 in HCC tissues was an independent risk factor indicating a poor prognosis (n = 145, P = 0.007). Combining the examination of serum PRDX6 with α-fetoprotein improved the diagnostic sensitivity of tests for HCC compared to α-fetoprotein alone (85.0% vs 50.0%, n = 40). We found that PRDX6 induced S phase arrest in HCC cells and inhibited HCC tumorigenicity in mice injected with cancer cells. When treated with H2 O2 , PRDX6 inhibited apoptosis. When treated with tumor necrosis factor alpha (TNF-α), PRDX6 promoted apoptosis. Inhibition of iPLA2 activity of PRDX6 decreased the apoptosis induced by TNF-α. In conclusion, PRDX6 inhibited the carcinogenesis of HCC, and the iPLA2 activity of PRDX6 promoted cancer cell death induced by TNF-α. © 2015 Wiley Periodicals, Inc.

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Investigating transcriptional regulation of Prdx6 in mouse liver cells

Cited by 56 publications

References 41 publications

Induction of Prdx1 and Prdx6 in Liver Cells by Serum and TPA

Induction of Prdx1 and Prdx6 in Liver Cells by Serum and TPA

Structure and Function of the Human Peroxiredoxin‐Based Antioxidant System: the Interplay between Peroxiredoxins, Thioredoxins, Thioredoxin Reductases, Sulfiredoxins and Sestrins

The phospholipase A2 activity of peroxiredoxin 6 promotes cancer cell death induced by tumor necrosis factor alpha in hepatocellular carcinoma

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