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001-es BibID:BIBFORM070379
Első szerző:Agod Zsófia
Cím:Regulation of type I interferon responses by mitochondria-derived reactive oxygen species in plasmacytoid dendritic cells / Zsofia Agod, Tünde Fekete, Marietta M. Budai, Aliz Varga, Attila Szabo, Hyelim Moon, István Boldogh, Tamás Biro, Árpád Lanyi, Attila Bacsi, Kitti Pazmandi
Dátum:2017
ISSN:2213-2317
Megjegyzések:Mitochondrial reactive oxygen species (mtROS) generated continuously under physiological conditions have recently emerged as critical players in the regulation of immune signaling pathways. In this study we have investigated the regulation of antiviral signaling by increased mtROS production in plasmacytoid dendritic cells (pDCs), which, as major producers of type I interferons (IFN), are the key coordinators of antiviral immunity. The early phase of type I IFN production in pDCs is mediated by endosomal Toll-like receptors (TLRs), whereas the late phase of IFN response can also be triggered by cytosolic retinoic acid-inducible gene-I (RIG-I), expression of which is induced upon TLR stimulation. Therefore, pDCs provide an ideal model to study the impact of elevated mtROS on the antiviral signaling pathways initiated by receptors with distinct subcellular localization. We found that elevated level of mtROS alone did not change the phenotype and the baseline cytokine profile of resting pDCs. Nevertheless increased mtROS levels in pDCs lowered the TLR9-induced secretion of pro-inflammatory mediators slightly, whereas reduced type I IFN production markedly via blocking phosphorylation of interferon regulatory factor 7 (IRF7), the key transcription factor of the TLR9 signaling pathway. The TLR9-induced expression of RIG-I in pDCs was also negatively regulated by enhanced mtROS production. On the contrary, elevated mtROS significantly augmented the RIG-I-stimulated expression of type I IFNs, as well as the expression of mitochondrial antiviral-signaling (MAVS) protein and the phosphorylation of Akt and IRF3 that are essential components of RIG-I signaling. Collectively, our data suggest that increased mtROS exert diverse immunoregulatory functions in pDCs both in the early and late phase of type I IFN responses depending on which type of viral sensing pathway is stimulated.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Plasmacytoid dendritic cell
Endosomal TLR signaling
Mitochondrial ROS
RIG-I signaling
Type I interferon
Megjelenés:Redox Biology. - 13 (2017), p. 633-645. -
További szerzők:Fekete Tünde (1984-) (immunológus, molekuláris biológus, mikrobiológus) Budai Marietta Margit (1985-) (molekuláris biológus) Varga Alíz (1983-) (immunológus) Szabó Attila (1981-) (molekuláris biológus, immunológus, filozófus) Moon, Hyelim Boldogh István Bíró Tamás (1968-) (élettanász) Lányi Árpád (1962-) (biológus, immunológus) Bácsi Attila (1967-) (immunológus) Pázmándi Kitti Linda (1984-) (molekuláris biológus, immunológus)
Pályázati támogatás:NKFIH PD 115776
Egyéb
NKFIH PD_16 120887
Egyéb
NKFIH K 125337
Egyéb
PNCDI II 119/2014
Egyéb
GINOP-2.3.2-15-2016-00050
GINOP
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2.

001-es BibID:BIBFORM076050
035-os BibID:(WoS)000447820100006 (Scopus)85048764575
Első szerző:Hao, Wenjing
Cím:Effects of the stimuli-dependent enrichment of 8-oxoguanine DNA glycosylase1 on chromatinized DNA / Hao Wenjing, Qi Tianyang, Pan Lang, Wang Ruoxi, Zhu Bing, Aguilera-Aguirre Leopoldo, Radak Zsolt, Hazra Tapas K., Vlahopoulos Spiros A., Bacsi Attila, Brasier Allan R., Ba Xueqing, Boldogh Istvan
Dátum:2018
ISSN:2213-2317
Megjegyzések:8-Oxoguanine DNA glycosylase 1 (OGG1) initiates the base excision repair pathway by removing one of the most abundant DNA lesions, 8-oxo-7,8-dihydroguanine (8-oxoG). Recent data showed that 8-oxoG not only is a promutagenic genomic base lesion, but also functions as an epigenetic mark and that consequently OGG1 acquire distinct roles in modulation of gene expression. In support, lack of functional OGG1 in Ogg1(-/-) mice led to an altered expression of genes including those responsible for the aberrant innate and adaptive immune responses and susceptibility to metabolic disorders. Therefore, the present study examined stimulus-driven OGG1-DNA interactions at whole genome level using chromatin immunoprecipitation (ChIP)-coupled sequencing, and the roles of OGG1 enriched on the genome were validated by molecular and system-level approaches. Results showed that signaling levels of cellular ROS generated by TNF alpha, induced enrichment of OGG1 at specific sites of chromatinized DNA, primarily in the regulatory regions of genes. OGG1-ChIP-ed genes are associated with important cellular and biological processes and OGG1 enrichment was limited to a time scale required for immediate cellular responses. Prevention of OGG1-DNA interactions by siRNA depletion led to modulation of NF-kappa B's DNA occupancy and differential expression of genes. Taken together these data show TNF alpha-ROS-driven enrichment of OGG1 at gene regulatory regions in the chromatinized DNA, which is a prerequisite to modulation of gene expression for prompt cellular responses to oxidant stress.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Redox Biology. - 18 (2018), p. 43-53. -
További szerzők:Qi, Tianyang Pan, Lang Wang, Ruoxi Zhu, Bing Aguilera-Aguirre, Leopoldo Radák Zsolt Hazra, Tapas K. Vlahopoulos, Spiros A. Bácsi Attila (1967-) (immunológus) Brasier, Allan R. Ba, Xueqing Boldogh István
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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