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1.

001-es BibID:BIBFORM065605
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Whole transcriptome analysis reveals an 8-oxoguanine DNA glycosylase-1-driven DNA repair-dependent gene expression linked to essential biological processes / Leopoldo Aguilera-Aguirre, Koa Hosoki, Attila Bacsi, Zsolt Radák, Thomas G. Wood, Steven G. Widen, Sanjiv Sur, Bill T. Ameredes, Alfredo Saavedra-Molina, Allan R. Brasier, Xueqing Ba, Istvan Boldogh
Dátum:2015
ISSN:0891-5849
Megjegyzések:Reactiveoxygenspeciesinflict oxidativemodifications onvariousbiologicalmolecules,includingDNA.One ofthemostabundantDNAbaselesions,8-oxo-7,8-dihydroguanine(8-oxoG)isrepairedby8-oxoguanineDNAglycosylase-1(OGG1)duringDNAbaseexcisionrepair(OGG1-BER).8-OxoGaccumula-tion inDNAhasbeenassociatedwithvariouspathologicalandagingprocesses,althoughitsroleisunclear.ThelackofOGG1-BERin Ogg1 / mice resultedindecreasedinflammatory responsesandincreased susceptibilitytoinfectionsandmetabolicdisorders.Therefore,weproposedthatOGG1and/or8-oxoGbasemayhavearoleinimmuneandhomeostaticprocesses.Totestourhypothesis,wechallenged mouselungswithOGG1-BERproduct8-oxoGbaseandchangesingeneexpressionweredetermined byRNAsequencinganddatawereanalyzedbyGeneOntologyandstatisticaltools.RNA-Seqanalysisidentified 1592differentiallyexpressed(Z 3-fold change)transcripts.TheupregulatedmRNAswererelatedtobiologicalprocesses,includinghomeostatic,immune-system,macrophageactivation,regulation ofliquid-surfacetension,andresponsetostimulus.Theseprocessesweremediatedbychemokines, cytokines,gonadotropin-releasinghormonereceptor,integrin,andinterleukinsignalingpathways.Takentogether,these findings pointtoanewparadigmshowingthatOGG1-BERplaysarolein variousbiologicalprocessesthatmaybenefit thehost,butwheninexcesscouldbeimplicatedindisease and/oragingprocesses.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
OGG1-BER
8-Oxoguanine
Gene expression
Biological processes
Megjelenés:Free Radical Biology And Medicine. - 81 (2015), p. 107-118. -
További szerzők:Hosoki, Koa Bácsi Attila (1967-) (immunológus) Radák Zsolt Wood, Thomas G. Widen, Steven G. Sur, Sanjiv Ameredes, Bill T. Saavedra-Molina, Alfredo Brasier, Allan R. Ba, Xueqing Boldogh István
Pályázati támogatás:TAMOP4.2.2.A-11/1/KONV- 2012?2023
Egyéb
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2.

001-es BibID:BIBFORM047646
035-os BibID:PMID:16298690
Első szerző:Bácsi Attila (immunológus)
Cím:Modulation of DNA-dependent protein kinase activity in chlorambucil-treated cells / Attila Bacsi, Subbaraj Kannan, Myung-Soog Lee, Tapas K. Hazra, Istvan Boldogh
Dátum:2005
ISSN:0891-5849
Megjegyzések:DNA-dependent protein kinase (DNA-PK) is activated in a two-step process whereby the Ku heterodimer first binds to the DNA double-strandbreaks (dsbs) and then the DNA-PK catalytic subunit (cs) is recruited to form a repair complex. Oxidative stress is simultaneously generated alongwith DNA damage by ionizing radiation or chemotherapeutic agents whose impact on the DNA-PK activity has not previously been investigated.Here we show that the DNA damage-induced kinase activity of DNA-PK was modulated by oxidative stress, which was induced along with DNAdsbs in chlorambucil (Cbl)-exposed cells. Pretreatment with the antioxidants, 2(3)-t-butyl-4-hydroxyanisole or N-acetyl-l-cysteine enhanced theamount of DNA-PKcs phosphorylated at threonine 2609 (DNA-PKpThr2609) at the DNA dsbs and DNA-PK activity. Conversely, oxidative stressinduced by l-buthionine (SR)-sulfoximine or glucose oxidase decreased the DNA-PK activity in Cbl-exposed cells. In addition, DNA-PKpThr2609was poorly detectable at the site of DNA dsbs, as shown by colocalization to DNA-end-binding pH2AX or p53BP1. There was no change in theprotein levels of DNA-PKcs, Ku70, or Ku86. Data from these studies provide the first evidence that oxidative stress effects posttranslationalmodification and assembly of DNA-PK complex at DNA dsbs, and thereby repair of DNA dsbs.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Oxidative stress
DNA-PK
DNA dsbs repair
Free radicals
Megjelenés:Free Radical Biology and Medicine. - 39 : 12 (2005), p. 1650-1659. -
További szerzők:Kannan, Subbaraj Myung-Soog, Lee Hazra, Tapas K. Boldogh István
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3.

001-es BibID:BIBFORM030561
Első szerző:Hajas György (biológus)
Cím:Biochemical identification of a hydroperoxide derivative of the free 8-oxo-7,8-dihydroguanine base / Gyorgy Hajas, Attila Bacsi, Leopoldo Aguilerra-Aguirre, Peter German, Zsolt Radak, Sanjiv Sur, Tapas K. Hazra, Istvan Boldogh
Dátum:2012
ISSN:0891-5849
Megjegyzések:-Oxo-7,8-dihydroguanine is one the most abundant base lesions in pro- and eukaryotic DNA. In mammalian cells, it is excised by the 8-oxoguanine DNA glycosylase (OGG1) during DNA base-excision repair, and the generated free 8-oxoG base is one of the DNA-derived biomarkers of oxidative stress in biological samples. The modification of 8-oxoG in the context of nucleoside and DNA has been the subject of many studies; however, the oxidative transformation of the free 8-oxoG base has not been described. By using biochemical and cell biological assays, we show that in the presence of molecular oxygen, the free 8-oxoG base transforms to a highly reactive hydroperoxide (8-oxoG*). Specifically, 8-oxoG* oxidizes Amplex red to resorufin, H(2)DCF to DCF, Fe(2+) to Fe(3+), and GSH to GSSG. This property of 8-oxoG* was diminished by treatment with catalase and glutathione peroxidase, but not superoxide dismutase. 8-OxoG* formation was prevented by reducing agents or nitrogen atmosphere. Its addition to CM-H(2)DCF-DA-loaded cells rapidly increased intracellular DCF fluorescence. There were no such properties observed for 8-oxodeoxyguanosine, 2,6-diamino-4-hydroxy-5-formamidopyrimidine, 2'-deoxyguanosine, guanine, adenine, guanosine, and 8-hydroxyadenine. These data imply that a free 8-oxoG base is more susceptible to oxidation than is its nucleoside form and, consequently, it stands as unique among intact and oxidatively modified purines.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekuláris Medicina
Free 8-oxoguanine base
Oxidative stress
Free radicals
külföldön készült közlemény
Megjelenés:Free Radical Biology And Medicine 52 : 4 (2012), p. 749-756. -
További szerzők:Bácsi Attila (1967-) (immunológus) Aguilera-Aguirre, Leopoldo Germán Péter (gyermekgyógyász) Radák Zsolt Sur, Sanjiv Hazra, Tapas K. Boldogh István
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
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4.

001-es BibID:BIBFORM055557
Első szerző:Luo, Jixian
Cím:8-Oxoguanine DNA glycosylase-1-mediated DNA repair is associated with Rho GTPase activation and α-smooth muscle actin polymerization / Jixian Luo, Koa Hosoki, Attila Bacsi, Zsolt Radak, Muralidhar L. Hegde, Sanjiv Sur, Tapas K. Hazra, Allan R. Brasier, Xueqing Ba, Istvan Boldogh
Dátum:2014
ISSN:0891-5849
Megjegyzések:Reactive oxygen species (ROS) are activators of cell signaling and modify cellular molecules, including DNA. 8-Oxo-7,8-dihydroguanine (8-oxoG) is one of the prominent lesions in oxidatively damaged DNA, whose accumulation is causally linked to various diseases and aging processes, whereas its etiological relevance is unclear. 8-OxoG is repaired by the 8-oxoguanine DNA glycosylase-1 (OGG1)-initiated DNA base excision repair (BER) pathway. OGG1 binds free 8-oxoG and this complex functions as an activator of Ras family GTPases. Here we examined whether OGG1-initiated BER is associated with the activation of Rho GTPase and mediates changes in the cytoskeleton. To test this possibility, we induced OGG1-initiated BER in cultured cells and mouse lungs and used molecular approaches such as active Rho pull-down assays, siRNA ablation of gene expression, immune blotting, and microscopic imaging. We found that OGG1 physically interacts with Rho GTPase and, in the presence of 8-oxoG base, increases Rho-GTP levels in cultured cells and lungs, which mediates ?-smooth muscle actin (?-SMA) polymerization into stress fibers and increases the level of ?-SMA in insoluble cellular/tissue fractions. These changes were absent in cells lacking OGG1. These unexpected data and those showing that 8-oxoG repair is a lifetime process suggest that, via Rho GTPase, OGG1 could be involved in the cytoskeletal changes and organ remodeling observed in various chronic diseases.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Free Radical Biology and Medicine. - 73 (2014), p. 430-438. -
További szerzők:Hosoki, Koa Bácsi Attila (1967-) (immunológus) Radák Zsolt Hegde, Muralidhar L. Sur, Sanjiv Hazra, Tapas K. Brasier, Allan R. Ba, Xueqing Boldogh István
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5.

001-es BibID:BIBFORM080824
Első szerző:Pázmándi Kitti Linda (molekuláris biológus, immunológus)
Cím:Oxidized base 8-oxoguanine, a product of DNA repair processes, contributes to dendritic cell activation / Kitti Pázmándi, Máté Sütő, Tünde Fekete, Aliz Varga, Eszter Boldizsár, István Boldogh, Attila Bácsi
Dátum:2019
Megjegyzések:A growing body of evidence suggests that elevated levels of reactive oxygen species (ROS) in the airways caused by exposure to gas phase pollutants or particulate matter are able to activate dendritic cells (DCs); however, the exact mechanisms are still unclear. When present in excess, ROS can modify macromolecules including DNA. One of the most abundant DNA base lesions is 7,8-dihydro-8-oxoguanine (8-oxoG), which is repaired by the 8-oxoguanine DNA glycosylase 1 (OGG1)-initiated base excision repair (BER) (OGG1-BER) pathway. Studies have also demonstrated that in addition to its role in repairing oxidized purines, OGG1 has guanine nucleotide exchange factor activity when bound to 8-oxoG. In the present study, we tested the hypothesis that exposure to 8-oxoG, the specific product of OGG1-BER, induces functional changes of DCs. Supporting our hypothesis, transcriptome analysis revealed that in mouse lungs, out of 95 genes associated with DCs' function, 22 or 42 were significantly upregulated after a single or multiple intranasal 8-oxoG challenges, respectively. In a murine model of allergic airway inflammation, significantly increased serum levels of ovalbumin (OVA)-specific IgE antibodies were detected in mice sensitized via nasal challenges with OVA+8-oxoG compared to those challenged with OVA alone. Furthermore, exposure of primary human monocyte-derived DCs (moDC) to 8-oxoG base resulted in significantly enhanced expression of cell surface molecules (CD40, CD86, CD83, HLA-DQ) and augmented the secretion of pro-inflammatory mediators IL-6, TNF and IL-8, whereas it did not considerably influence the production of the anti-inflammatory cytokine IL-10. The stimulatory effects of 8-oxoG on human moDCs were abolished upon siRNA-mediated OGG1 depletion. Collectively, these data suggest that OGG1-BER-generated 8-oxoG base-driven cell signaling activates DCs, which may contribute to initiation of both the innate and adaptive immune responses under conditions of oxidative stress.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Free Radical Biology and Medicine. - 143 (2019), p. 209-220. -
További szerzők:Sütő Máté István (1991-) (molekuláris biológus) Fekete Tünde (1984-) (immunológus, molekuláris biológus, mikrobiológus) Varga Alíz (1983-) (immunológus) Boldizsár Eszter Boldogh István Bácsi Attila (1967-) (immunológus)
Pályázati támogatás:EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
GINOP-2.3.2-15-2016-00050
GINOP
NKFIH K 109595
OTKA
NKFIH K 125337
OTKA
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6.

001-es BibID:BIBFORM055554
Első szerző:Pázmándi Kitti Linda (molekuláris biológus, immunológus)
Cím:Oxidative modification enhances the immunostimulatory effects of extracellular mitochondrial DNA on plasmacytoid dendritic cells / Kitti Pazmandi, Zsofia Agod, Brahma V. Kumar, Attila Szabo, Tunde Fekete, Viktoria Sogor, Agota Veres, Istvan Boldogh, Eva Rajnavolgyi, Arpad Lanyi, Attila Bacsi
Dátum:2014
ISSN:0891-5849
Megjegyzések:Inflammation is associated with oxidative stress and characterized by elevated levels of damage-associated molecular pattern (DAMP) molecules released from injured or even living cells into the surrounding microenvironment. One of these endogenous danger signals is the extracellular mitochondrial DNA (mtDNA) containing evolutionary conserved unmethylated CpG repeats. Increased levels of reactive oxygen species (ROS) generated by recruited inflammatory cells modify mtDNA oxidatively resulting primarily in accumulation of 8-oxo-7,8-dihydroguanine (8-oxoG) lesions. In this study, we examined the impact of native and oxidatively modified mtDNAs on the phenotypic and functional properties of plasmacytoid dendritic cells (pDCs), which possess a fundamental role in the regulation of inflammation and T cell immunity. Treatment of human primary pDCs with native mtDNA up-regulated the expression of a co-stimulatory molecule (CD86), a specific maturation marker (CD83), and a main antigen-presenting molecule (HLA-DQ) on the cell surface, as well as increased TNF-? and IL-8 production from the cells. These effects were more apparent when pDCs were exposed to oxidatively modified mtDNA. Neither native nor oxidized mtDNA molecules were able to induce interferon (IFN)-? secretion from pDCs unless they formed a complex with human cathelicidin LL-37, an antimicrobial peptide. Interestingly, simultaneous administration of a Toll-like receptor (TLR)9 antagonist abrogated the effects of both native and oxidized mtDNAs on human pDCs. In a murine model, oxidized mtDNA also proved a more potent activator of pDCs compared to the native form, except for induction of IFN-? production. Collectively, we demonstrate here for the first time that elevated levels of 8-oxoG bases in the extracellular mtDNA induced by oxidative stress increase the immunostimulatory capacity of mtDNA on pDCs.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Plasmacytoid dendritic cells
Extracellular mitochondrial DNA
Oxidative stress
8-oxoguanine base
Inflammation
Megjelenés:Free Radical Biology and Medicine. - 77 (2014), p. 281-290. -
További szerzők:Agod Zsófia Kumar, Brahma V. Szabó Attila (1981-) (molekuláris biológus, immunológus, filozófus) Fekete Tünde (1984-) (immunológus, molekuláris biológus, mikrobiológus) Somogyi Viktória (1989-) (biotechnológus) Veres Ágota (laboráns) Boldogh István Rajnavölgyi Éva (1950-) (immunológus) Lányi Árpád (1962-) (biológus, immunológus) Bácsi Attila (1967-) (immunológus)
Pályázati támogatás:K-109595
OTKA
TAMOP-4.2.2.A-11/1/KONV-2012-0023
TÁMOP
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7.

001-es BibID:BIBFORM030562
Első szerző:Pázmándi Kitti Linda (molekuláris biológus, immunológus)
Cím:Modulatory effects of low-dose hydrogen peroxide on the function of human plasmacytoid dendritic cells / Kitti Pazmandi, Zoltan Magyarics, Istvan Boldogh, Aniko Csillag, Eva Rajnavolgyi, Attila Bacsi
Dátum:2012
ISSN:0891-5849
Megjegyzések:Under normal conditions, plasmacytoid dendritic cells (pDCs) are located in peripheral lymphoid organs or circulate in the blood, from where they can migrate to sites of infection or inflammation. In inflamed tissues, pDCs can be exposed to elevated levels of reactive oxygen species produced by inflammatory cells and we presume that oxidative stress could affect the cellular responses of pDCs to microenvironmental stimuli. To explore this possibility, human pDCs isolated from peripheral blood of healthy donors were treated with H(2)O(2) and R837 (a Toll-like receptor 7 ligand), separately and in combination. Our results demonstrate that treatment with a low concentration (0.01?M) of H(2)O(2) resulted in only slight changes in the expression of CD40, CD80, CD86, and CD83; however, low-dose H(2)O(2) markedly decreased the expression of HLA-DQ on pDCs. Exposure to H(2)O(2) did not trigger the release of IL-6, TNF-?, IL-8, or IFN-? from pDCs. Although addition of H(2)O(2) did not modify the capacity of pDCs to activate allogeneic IL-17- or IFN-?-producing T cells, it significantly increased the ability of pDCs to stimulate IL-4-secreting T cells. Exposure of pDCs to H(2)O(2) before cocultivation with naïve autologous T cells significantly lowered IL-10 production by T cells, but did not affect IL-17 release. It was also observed that H(2)O(2)-exposed pDCs provided stronger stimuli for Th2 than for Th1 differentiation upon autologous activation, compared to untreated pDCs, possibly because of elevated surface expression of OX40-L. Most importantly, when pDCs were stimulated with R837 in the presence of H(2)O(2), decreased phenotypic activation, decreased chemokine and cytokine release, and impaired allo- and autostimulatory functions of pDCs were detected, indicating that pDCs exposed to oxidative stress in vivo may have an anti-inflammatory or tolerogenic role in regulating adaptive immune responses.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekuláris Medicina
Plasmacytoid dendritic cells
Oxidative stress
Inflammation
Immune regulation
Free radicals
egyetemen (Magyarországon) készült közlemény
Megjelenés:Free Radical Biology and Medicine 52 : 3 (2012), p. 635-645. -
További szerzők:Magyarics Zoltán (1982-) (immunológus) Boldogh István Csillag Anikó (1979-) (immunológus, biológus, angol-magyar szakfordító) Rajnavölgyi Éva (1950-) (immunológus) Bácsi Attila (1967-) (immunológus)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Molekuláris immunológia
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8.

001-es BibID:BIBFORM037368
Első szerző:Robaszkiewicz, Agnieszka (biokémikus)
Cím:Hydrogen peroxide-induced poly(ADP-ribosyl)ation regulates osteogenic differentiation-associated cell death / Robaszkiewicz Agnieszka, Erdélyi Katalin, Kovács Katalin, Kovács István, Bai Péter, Rajnavölgyi Éva, Virág László
Dátum:2012
ISSN:0891-5849
Megjegyzések:We set out to investigate the role of poly(ADP-ribosylation), the attachment of NAD(+)-derived (ADP-ribose)(n) polymers to proteins, in the regulation of osteogenic differentiation of SAOS-2 cells and mesenchymal stem cells. In osteogenic differentiation medium, SAOS-2 cells showed mineralization and expressed alkaline phosphatase and osteoblastic marker genes such as Runx2, osterix, BMP2, and osteopontin. The cells also released hydrogen peroxide, displayed poly(ADP-ribose) polymerase (PARP) activation, and showed commitment to cell death (apoptosis and necrosis). Scavenging reactive oxygen species by glutathione or decomposing hydrogen peroxide by the addition of catalase reduced differentiation, PARP activation, and cell death. We silenced the expression of the main PAR-synthesizing enzyme PARP-1 and the PAR-degrading enzyme poly(ADP-ribose) glycohydrolase (PARG) in SAOS-2 osteosarcoma cells (shPARP-1 and shPARG, respectively). Both shPARP-1- and shPARG-silenced cells exhibited altered differentiation, with the most notable change being increased osteopontin expression but decreased alkaline phosphatase activity. PARP-1 silencing suppressed both apoptotic and necrotic cell death, but the PARP inhibitor PJ34 sensitized cells to cell death, indicating that the effects of PARP-1 silencing are not related to the activity of the enzyme. PARG silencing resulted in more apoptosis and, in the last days of differentiation, a shift from apoptosis toward necrosis. In conclusion our data prove that hydrogen peroxide-induced poly(ADP-ribose) signaling regulates cell death and osteodifferentiation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekuláris Medicina
Megjelenés:Free Radical Biology And Medicine. - 53 : 8 (2012), p. 1552-1564. -
További szerzők:Erdélyi Katalin (1978-) (molekuláris biológus, biokémikus) Kovács Katalin (1978-) (biokémikus) Kovács István (1985-) (biokémikus) Bai Péter (1976-) (biokémikus) Rajnavölgyi Éva (1950-) (immunológus) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus)
Pályázati támogatás:K82009
OTKA
K75864
OTKA
PD83473
OTKA
TÁMOP-4.2.2.A-11/1/KONV-2012-0025
TÁMOP
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Oxidatív stressz és ADP-riboziláció kapcsolatának vizsgálata
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Jelátviteli kapcsolatok ős- és dendritikus sejt altípusokban
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
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