Inhibitory role of peroxiredoxin II (Prx II) on cellular senescence

Han, Ying‐Hao; Kim, Hyunsun; Kim, Jin Man; Kim, Sang-Keun; Yu, Dae‐Yeul; Moon, Eun‐Yi

doi:10.1016/j.febslet.2005.07.049

Cited by 65 publications

(54 citation statements)

References 34 publications

(46 reference statements)

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“…cellular senescence and aging. 43 In addition, Prdx2 has been reported to have an important role in the inhibition of apoptosis in a novel pathway distinct from Bcl-2. 44,45 The increased expression of Prdx2 following treatment with pCons might shed light on the mechanism by which peptide tolerization decreases apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Distinct gene signature revealed in white blood cells, CD4+ and CD8+ T cells in (NZBx NZW) F1 lupus mice after tolerization with anti-DNA Ig peptide

et al. 2010

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Tolerizing mice polygenically predisposed to lupus-like disease (NZB/NZW F1 females) with a peptide mimicking anti-DNA IgG sequences containing MHC class I and class II T cell determinants (pConsensus, pCons) results in protection from full-blown disease attributable in part to the induction of CD4 þ CD25 þ Foxp3 þ and CD8 þ Foxp3 þ regulatory T cells. We compared 45 000 murine genes in total white blood cells (WBC), CD4 þ T cells, and CD8 þ T cells from splenocytes of (NZBxNZW) F1 lupus-prone mice tolerized with pCons vs untreated naïve mice and found two-fold or greater differential expression for 448 WBC, 174 CD4, and 60 CD8 genes. We identified differentially expressed genes that played roles in the immune response and apoptosis. Using real-time PCR, we validated differential expression of selected genes (IFI202B, Bcl2, Foxp3, Trp-53, CCR7 and IFNar1) in the CD8 þ T cell microarray and determined expression of selected highly upregulated genes in different immune cell subsets. We also determined Smads expression in different immune cell subsets, including CD4 þ T cells and CD8 þ T cells, to detect the effects of TGF-b, known to be the major cytokine that accounts for the suppressive capacity of CD8 þ Treg in this system. Silencing of anti-apoptotic gene Bcl2 or interferon genes (IFI202b and IFNar1 in combination) in CD8 þ T cells from tolerized mice did not affect the expression of the other selected genes. However, silencing of Foxp3 reduced expression of Foxp3, Ifi202b and PD1-all of which are involved in the suppressive capacity of CD8 þ Treg in this model.

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Section: Discussionmentioning

confidence: 99%

Distinct gene signature revealed in white blood cells, CD4+ and CD8+ T cells in (NZBx NZW) F1 lupus mice after tolerization with anti-DNA Ig peptide

et al. 2010

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“…Prx II regulates cellular senescence and aging. Prx II null mouse embryo fibroblasts showed elevated levels of reactive oxygen species (ROS) and cellular senescence, and Prx II null mice showed signs of accelerated skin aging (38). p53 overexpression induces ROS production, resulting in oxidative degradation of mitochondrial components followed by apoptotic cell death (39).…”

Section: Relationship Between Protein Expression Changes and Apoptosismentioning

confidence: 99%

p53 targets identified by protein expression profiling

Rahman-Roblick

Roblick

Hellman

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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p53 triggers cell cycle arrest and apoptosis through transcriptional regulation of specific target genes. We have investigated the effect of p53 activation on the proteome using 2D gel electrophoresis analysis of mitomycin C-treated HCT116 colon carcinoma cells carrying wild-type p53. Approximately 5,800 protein spots were separated in overlapping narrow-pH-range gel strips, and 115 protein spots showed significant expression changes upon p53 activation. The identity of 55 protein spots was obtained by mass spectrometry. The majority of the identified proteins have no previous connection to p53. The proteins fall into different functional categories, such as mRNA processing, translation, redox regulation, and apoptosis, consistent with the idea that p53 regulates multiple cellular pathways. p53-dependent regulation of five of the up-regulated proteins, eIF5A, hnRNP C1/C2, hnRNP K, lamin A/C, and Nm23-H1, and two of the down-regulated proteins, Prx II and TrpRS, was examined in further detail. Analysis of mRNA expression levels demonstrated both transcription-dependent and transcription-independent regulation among the identified targets. Thus, this study reveals protein targets of p53 and highlights the role of transcription-independent effects for the p53-induced biological response.proteomics ͉ transcription factor ͉ cancer

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“…It is important to highlight that animals lacking PRDX1 are tumor prone, their life span is reduced [123], and their tissues contain elevated levels of damaged DNA [124]. Additionally, cellular senescence is accelerated in PRDX2 −/− mouse embryonic fibroblasts [125]. In these two knockout animals, severe anaemia is seen as part of the phenotype [108,123].…”

Section: Prdx4mentioning

confidence: 99%

The Enzymatic Antioxidant System of Human Spermatozoa

O’Flaherty

2014

Advances in Andrology

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The ejaculated spermatozoon, as an aerobic cell, must fight against toxic levels of reactive oxygen species (ROS) generated by its own metabolism but also by other sources such as abnormal spermatozoa, chemicals and toxicants, or the presence of leukocytes in semen. Mammalian spermatozoa are extremely sensitive to oxidative stress, a condition occurring when there is a net increase in ROS levels within the cell. Opportunely, this specialized cell has a battery of antioxidant enzymes (superoxide dismutase, peroxiredoxins, thioredoxins, thioredoxins reductases, and glutathione s-transferases) working in concert to assure normal sperm function. Any impairment of the antioxidant enzymatic activities will promote severe oxidative damage which is observed as plasma membrane lipid peroxidation, oxidation of structural proteins and enzymes, and oxidation of DNA bases that lead to abnormal sperm function. Altogether, these damages occurring in spermatozoa are associated with male infertility. The present review contains a description of the enzymatic antioxidant system of the human spermatozoon and a reevaluation of the role of its different components and highlights the necessity of sufficient supply of reducing agents (NADPH and reduced glutathione) to guarantee normal sperm function.

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Inhibitory role of peroxiredoxin II (Prx II) on cellular senescence

Cited by 65 publications

References 34 publications

Distinct gene signature revealed in white blood cells, CD4+ and CD8+ T cells in (NZBx NZW) F1 lupus mice after tolerization with anti-DNA Ig peptide

Distinct gene signature revealed in white blood cells, CD4+ and CD8+ T cells in (NZBx NZW) F1 lupus mice after tolerization with anti-DNA Ig peptide

p53 targets identified by protein expression profiling

The Enzymatic Antioxidant System of Human Spermatozoa

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