CCL

Összesen 12 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM072833
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Pollen-induced oxidative DNA damage response regulates miRNAs controlling allergic inflammation / Aguilera-Aguirre Leopoldo, Hao Wenging, Pan Lang, Li Xiaoxue, Saavedra-Molina Alfredo, Bacsi Attila, Radak Zsolt, Sur Sanjiv, Brasier Allan R., Ba Xueqing, Boldogh Istvan
Dátum:2017
ISSN:1040-0605 1522-1504
Megjegyzések:A mucosal oxidative burst is a hallmark response to pollen exposure that promotes allergic inflammatory responses. Reactive species constituents of oxidative stress signal via the modification of cellular molecules including nucleic acids. One of the most abundant forms of oxidative genomic base damage is 8-oxo-7,8-dihydroguanine (8-oxoG), which is removed from DNA by 8-oxoguanine DNA glycosylase 1 (OGG1). OGG1 in complex with 8-oxoG acts as a GDP-GTP exchange factor and induces acute inflammation; however, the mechanism(s) by which OGG1 signaling regulates allergic airway inflammation is not known. Here, we postulate that the OGG1 signaling pathway differentially altered the levels of small regulatory RNAs and increased the expression of T helper 2 (Th2) cytokines in ragweed pollen extract (RWPE)-challenged lungs. To determine this, the lungs of sensitized mice expressing or lacking OGG1 were challenged with RWPE and/or with OGG1's excision product 8-oxoG. The responses in lungs were assessed by next-generation sequencing, as well as various molecular and histological approaches. The results showed that RWPE challenge induced oxidative burst and damage to DNA and activated OGG1 signaling, resulting in the differential expression of 84 micro-RNAs (miRNAs), which then exacerbated antigen-driven allergic inflammation and histological changes in the lungs. The exogenous administration of the downregulated let-7b-p3 mimetic or inhibitors of upregulated miR-23a or miR-27a decreased eosinophil recruitment and mucus and collagen production via controlling the expression of IL-4, IL-5, and IL-13. Together, these data demonstrate the roles of OGG1 signaling in the regulation of antigen-driven allergic immune responses via differential expression of miRNAs upstream of Th2 cytokines and eosinophils.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
DNA repair
allergy
cell signaling
micro-RNAs
Megjelenés:American Journal Of Physiology-Lung Cellular And Molecular Physiology 313 : 6 (2017), p. L1058-L1068. -
További szerzők:Hao, Wenging Pan, Lang Li, Xiaoxue Saavedra-Molina, Alfredo Bácsi Attila (1967-) (immunológus) Radák Zsolt Sur, Sanjiv Brasier, Allan R. Ba, Xueqing Boldogh István
Pályázati támogatás:OTKA-109595
OTKA
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

2.

001-es BibID:BIBFORM065564
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Whole transcriptome analysis reveals a role for OGG1-initiated DNA repair signaling in airway remodeling / Leopoldo Aguilera-Aguirre, Koa Hosoki, Attila Bacsi, Zsolt Radák, Sanjiv Sur, Muralidhar L. Hegde, Bing Tian, Alfredo Saavedra-Molina, Allan R. Brasier, Xueqing Ba, Istvan Boldogh
Dátum:2015
ISSN:0891-5849
Megjegyzések:Reactive oxygen species (ROS) generated by environmental exposures, and endogenously as by-products of respiration, oxidatively modify biomolecules including DNA. Accumulation of ROS-induced DNA damage has been implicated in various diseases that involve inflammatory processes, and efficient DNA repair is considered critical in preventing such diseases. 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 (OGG1-BER) pathway. Recent studies have shown that the OGG1-BER by-product 8-oxoG base forms a complex with cytosolic OGG1, activating small GTPases and downstream cell signaling in cultured cells and lungs. This implies that persistent OGG1-BER could result in signaling leading to histological changes in airways. To test this, we mimicked OGG1-BER by repeatedly challenging airways with its repair product 8-oxoG base. Gene expression was analyzed by RNA sequencing (RNA-Seq) and qRT-PCR, and datasets were evaluated by gene ontology and statistical tools. RNA-Seq analysis identified 3252 differentially expressed transcripts (2435 up- and 817 downregulated, ? 3-fold change). Among the upregulated transcripts, 2080 mRNAs were identified whose encoded protein products were involved in modulation of the actin family cytoskeleton, extracellular matrix, cell adhesion, cadherin, and cell junctions, affecting biological processes such as tissue development, cell-to-cell adhesion, cell communication, and the immune system. These data are supported by histological observations showing epithelial alterations, subepithelial fibrosis, and collagen deposits in the lungs. These data imply that continuous challenge by the environment and consequent OGG1-BER-driven signaling trigger gene expression consistent with airway remodeling.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
8-Oxoguanine
Airway remodeling
OGG1-BER
Megjelenés:Free Radical Biology And Medicine 89 (2015), p. 20-33. -
További szerzők:Hosoki, Koa Bácsi Attila (1967-) (immunológus) Radák Zsolt Sur, Sanjiv Hegde, Muralidhar L. Tian, Bing Saavedra-Molina, Alfredo Brasier, Allan R. Ba, Xueqing Boldogh István
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

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
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

001-es BibID:BIBFORM055555
Első szerző:Aguilera-Aguirre, Leopoldo
Cím:Innate Inflammation Induced by the 8-Oxoguanine DNA Glycosylase-1-KRAS-NF-kB Pathway / Leopoldo Aguilera-Aguirre, Attila Bacsi, Zsolt Radak, Tapas K. Hazra, Sankar Mitra, Sanjiv Sur, Allan R. Brasier, Xueqing Ba, Istvan Boldogh
Dátum:2014
ISSN:0022-1767 1550-6606
Megjegyzések:8-Oxoguanine-DNA glycosylase-1 (OGG1) is the primary enzyme for repairing 7,8-dihydro-8-oxoguanine (8-oxoG) via the DNAbase excision repair pathway (OGG1-BER). Accumulation of 8-oxoG in the genomic DNA leads to genetic instability and carcinogenesis and is thought to contribute to the worsening of various inflammatory and disease processes. However, the disease mechanism is unknown. In this study, we proposed that the mechanistic link between OGG1-BER and proinflammatory gene expression is OGG1's guanine nucleotide exchange factor activity, acquired after interaction with the 8-oxoG base and consequent activationof the small GTPase RAS. To test this hypothesis, we used BALB/c mice expressing or deficient in OGG1 in their airwayepithelium and various molecular biological approaches, including active RAS pulldown, reporter and Comet assays, small interfering RNA?mediated depletion of gene expression, quantitative RT-PCR, and immunoblotting. We report that the OGG1-intiated repair of oxidatively damaged DNA is a prerequisite for GDP?GTP exchange, KRAS-GTP?driven signaling via MAP kinases and PI3 kinases and mitogen-stress?related kinase-1 for NF-kB activation, proinflammatory chemokine/cytokine expression, and inflammatory cell recruitment to the airways. Mice deficient in OGG1-BER showed significantly decreasedimmune responses, whereas a lack of other Nei-like DNA glycosylases (i.e., NEIL1 and NEIL2) had no significant effect. These data unveil a previously unidentified role of OGG1-driven DNA BER in the generation of endogenous signals for inflammation in the innate signaling pathway.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Immunology. - 193 : 9 (2014), p. 4643-4653. -
További szerzők:Bácsi Attila (1967-) (immunológus) Radák Zsolt Hazra, Tapas K. Mitra, Sankar Sur, Sanjiv Brasier, Allan R. Ba, Xueqing Boldogh István
Pályázati támogatás:TAMOP 4.2.2.A-11/1/KONV-2012-2023
TÁMOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

5.

001-es BibID:BIBFORM051534
035-os BibID:WOS:000332701400043
Első szerző:Ba, Xueqing
Cím:8-oxoguanine DNA glycosylase-1 augments proinflammatory gene expression by facilitating the recruitment of site-specific transcription factors / Xueqing Ba, Attila Bacsi, Jixian Luo, Leopoldo Aguilera-Aguirre, Xianlu Zeng, Zsolt Radak, Allan R. Brasier, Istvan Boldogh
Dátum:2014
ISSN:0022-1767 1550-6606
Megjegyzések:Among the insidious DNA base lesions, 8-oxo-7,8-dihydroguanine (8-oxoG) is one of the most abundant, a lesion that arises through the attack by reactive oxygen species on guanine, especially when located in cis-regulatory elements. 8-oxoG is repaired by the 8-oxoguanine glycosylase 1 (OGG1)-initiated DNA base excision repair pathway. In this study, we investigated whether 8-oxoG repair by OGG1 in promoter regions is compatible with a prompt gene expression and a host innate immune response. For this purpose, we used a mouse model of airway inflammation, supplemented with cell cultures, chromatin immunoprecipitation, small interfering RNA knockdown, real-time PCR, and comet and reporter transcription assays. Our data show that exposure of cells to TNF-? altered cellular redox, increased the 8-oxoG level in DNA, recruited OGG1 to promoter sequences, and transiently inhibited base excision repair of 8-oxoG. Promoter-associated OGG1 then enhanced NF-?B/RelA binding to cis-elements and facilitated recruitment of specificity protein 1, transcription initiation factor II-D, and p-RNA polymerase II, resulting in the rapid expression of chemokines/cytokines and inflammatory cell accumulation in mouse airways. Small interfering RNA depletion of OGG1 or prevention of guanine oxidation significantly decreased TNF-?-induced inflammatory responses. Taken together, these results show that nonproductive binding of OGG1 to 8-oxoG in promoter sequences could be an epigenetic mechanism to modulate gene expression for a prompt innate immune response.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
OGG1
8-oxoG
trans-ACTING FACTORS
INNATE IMMUNE RESPONSE
Megjelenés:Journal of Immunology. - 192 : 5 (2014), p. 2384-2394. -
További szerzők:Bácsi Attila (1967-) (immunológus) Luo, Jixian Aguilera-Aguirre, Leopoldo Zeng, Xianlu Radák Zsolt Brasier, Allan R. Boldogh István
Pályázati támogatás:4.2.2.A-11/1/KONV-2012-0023
TÁMOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

6.

001-es BibID:BIBFORM091749
Első szerző:Boldogh István
Cím:OGG1 at the Crossroads of Inflammation and DNA Base Excision Repair / I. Boldogh, L. Pan, S. Vlahopoulos, X. Zheng, K. Wang, T. K. Hazra, M. L. Hegde, A. Bacsi, Z. Radak, A. R. Brasier, X. Ba
Dátum:2020
Megjegyzések:Oxidative modification(s) to nucleic acid bases are an unavoidable consequence of reactions by reactive oxygen species. Arguably, the most abundant ROS-generated lesion in nuclear and mitochondrial DNA is 7, 8-dihydro-8-oxoguanine (8-oxoGua), which is repaired primarily by 8-oxoguanine DNA glycosylase 1, in the OGG1-initiated base excision repair pathway. Deficiency in OGG1 repair is believed to have role(s) in development and progression of various disease processes, including neurodegenerative, cardiovascular, metabolic diseases, and aging-associated pathologies. The common link among these diseases is acute/chronic inflammatory processes. Emerging data support the idea that OGG1-induced adjustments in DNA structure at genomic 8-oxoGua with or without excision, serve as a nucleation site for transcription factor binding allowing prompt expression of genes, essential for reestablishment of a homeostatic state via innate and adaptive immune responses after exposure to biological and/or cytotoxic agents. As part of the immune defenses, OGG1 in complex with a free 8-oxoGua base also exerts transcriptional control via small GTPase signaling pathways. These data are consistent with the limited immune responses of Ogg1 knockout mice. Thus, evolution integrated genome maintenance by OGG1-BER and control host homeostatic state via inflammation, which, if not controlled, can be one of the mechanistic explanations for OGG1's previously proposed link to diseases and aging processes.
ISBN:978-1-83916-251-0; 978-1-83916-254-1; 978-1-83916-256-5
Tárgyszavak:Természettudományok Biológiai tudományok könyvfejezet
könyvrészlet
OGG1
Megjelenés:DNA Damage, DNA Repair and Disease: Volume 2 / Eds. Miral Dizdaroglu, R. Stephen Lloyd. - p. 75-103. -
További szerzők:Pan, Lang Vlahopoulos, Spiros A. Zheng, Xiaoxiang Wang, K. Hazra, Tapas K. Hegde, Muralidhar L. Bácsi Attila (1967-) (immunológus) Radák Zsolt Brasier, Allan R. Ba, Xueqing
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

7.

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
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

8.

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
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

9.

001-es BibID:BIBFORM041840
Első szerző:Murai, Hiroki
Cím:Alternaria-Induced Release of IL-18 from Damaged Airway Epithelial Cells : n NF-kB Dependent Mechanism of Th2 Differentiation? / Hiroki Murai, Huibin Qi, Barun Choudhury, Jim Wild, Nilesh Dharajiya, Swapnil Vaidya, Anjana Kalita, Attila Bacsi, David Corry, Alexander Kurosky, Allan Brasier, Istvan Boldogh, Sanjiv Sur
Dátum:2012
Megjegyzések:BACKGROUND: A series of epidemiologic studies have identified the fungus Alternaria as a major risk factor for asthma. The airway epithelium plays a critical role in the pathogenesis of allergic asthma. These reports suggest that activated airway epithelial cells can produce cytokines such as IL-25, TSLP and IL-33 that induce Th2 phenotype. However the epithelium-derived products that mediate the pro-asthma effects of Alternaria are not well characterized. We hypothesized that exposure of the airway epithelium to Alternaria releasing cytokines that can induce Th2 differentiation.METHODOLOGY/PRINCIPAL FINDING: We used ELISA to measure human and mouse cytokines. Alternaria extract (ALT-E) induced rapid release of IL-18, but not IL-4, IL-9, IL-13, IL-25, IL-33, or TSLP from cultured normal human bronchial epithelial cells; and in the BAL fluids of naïve mice after challenge with ALT-E. Both microscopic and FACS indicated that this release was associated with necrosis of epithelial cells. ALT-E induced much greater IL-18 release compared to 19 major outdoor allergens. Culture of naïve CD4 cells with rmIL-18 induced Th2 differentiation in the absence of IL-4 and STAT6, and this effect was abrogated by disrupting NF- ?B p50 or with a NEMO binding peptide inhibitor.CONCLUSION/SIGNIFICANCE: Rapid and specific release of IL-18 from Alternaria-exposed damaged airway epithelial cells can directly initiate Th2 differentiation of naïve CD4(+) T-cells via a unique NF-?B dependent pathway.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:PLoS One. - 7 : 2 (2012), p. e30280. -
További szerzők:Qi, Huibin Choudhury, Barun K. Wild, Jim Dharajiya, Nilesh G. Vaidya, Swapnil Kalita, Anjana Bácsi Attila (1967-) (immunológus) Corry, David Kurosky, Alexander Brasier, Allan R. Boldogh István Sur, Sanjiv
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

10.

001-es BibID:BIBFORM114252
035-os BibID:(cikkazonosító)1186369 (scopus)85168475682 (wos)001052448900001
Első szerző:Pan, Lang
Cím:Substrate-specific binding of 8-oxoguanine DNA glycosylase 1 (OGG1) reprograms mucosal adaptations to chronic airway injury / Pan Lang, Vlahopoulos Spiros, Tanner Lloyd, Bergwik Jesper, Bacsi Attila, Radak Zsolt, Egesten Arne, Ba Xueqing, Brasier Allan R., Boldogh Istvan
Dátum:2023
ISSN:1664-3224
Megjegyzések:Recent advances have uncovered the non-random distribution of 7, 8-dihydro-8-oxoguanine (8-oxoGua) induced by reactive oxygen species, which is believed to have epigenetic effects. Its cognate repair protein, 8-oxoguanine DNA glycosylase 1 (OGG1), reads oxidative substrates and participates in transcriptional initiation. When redox signaling is activated in small airway epithelial cells, the DNA repair function of OGG1 is repurposed to transmit acute inflammatory signals accompanied by cell state transitions and modification of the extracellular matrix. Epithelial-mesenchymal and epithelial-immune interactions act cooperatively to establish a local niche that instructs the mucosal immune landscape. If the transitional cell state governed by OGG1 remains responsive to inflammatory mediators instead of differentiation, the collateral damage provides positive feedback to inflammation, ascribing inflammatory remodeling to one of the drivers in chronic pathologies. In this review, we discuss the substrate-specific read through OGG1 has evolved in regulating the innate immune response, controlling adaptations of the airway to environmental and inflammatory injury, with a focus on the reader function of OGG1 in initiation and progression of epithelial to mesenchymal transitions in chronic pulmonary disease.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Frontiers in Immunology. - 14 (2023), p. 1-12. -
További szerzők:Vlahopoulos, Spiros A. Tanner, Lloyd Bergwik, Jesper Bácsi Attila (1967-) (immunológus) Radák Zsolt Egesten, Arne Ba, Xueqing Brasier, Allan R. Boldogh István
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

11.

001-es BibID:BIBFORM069722
Első szerző:Pan, Lang
Cím:Oxidized Guanine Base Lesions Function in 8-Oxoguanine DNA Glycosylase-1-mediated Epigenetic Regulation of Nuclear Factor ?B-driven Gene Expression / Lang Pan, Bing Zhu, Wenjing Hao, Xianlu Zeng, Spiros A. Vlahopoulos, Tapas K. Hazra, Muralidhar L. Hegde, Zsolt Radak, Attila Bacsi, Allan R. Brasier, Xueqing Ba, Istvan Boldogh
Dátum:2016
ISSN:0021-9258 1083-351X
Megjegyzések:A large percentage of redox-responsive gene promoters containevolutionarily conserved guanine-rich clusters; guaninesare the bases most susceptible to oxidative modification(s). Consequently,7,8-dihydro-8-oxoguanine (8-oxoG) is one of themost abundant base lesions in promoters and is primarilyrepaired via the 8-oxoguanine DNA glycosylase-1 (OOG1)-initiatedbase excision repair pathway. In view of a prompt cellularresponse to oxidative challenge, we hypothesized that the8-oxoG lesion and the cognate repair protein OGG1 are utilizedin transcriptional gene activation. Here, we document TNF -induced enrichment of both 8-oxoG and OGG1 in promoters ofpro-inflammatory genes, which precedes interaction of NF- Bwith its DNA-binding motif. OGG1 bound to 8-oxoG upstreamfrom the NF- B motif increased its DNA occupancy by promotingan on-rate of both homodimeric and heterodimeric forms ofNF- B. OGG1 depletion decreased both NF- B binding andgene expression, whereas Nei-like glycosylase-1 and -2 had amarginal effect. These results are the first to document a novelparadigm wherein the DNA repair protein OGG1 bound to itssubstrate is coupled to DNA occupancy of NF- B and functionsin epigenetic regulation of gene expression.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
8-oxoguanine DNA glycosylase1
8-oxoguanine
NF-kappaB
gene expression
inflammation
Megjelenés:Journal Of Biological Chemistry 291 : 49 (2016), p. 25553-25566. -
További szerzők:Zhu, Bing Hao, Wenjing Zeng, Xianlu Vlahopoulos, Spiros A. Hazra, Tapas K. Hegde, Muralidhar L. Radák Zsolt Bácsi Attila (1967-) (immunológus) Brasier, Allan R. Ba, Xueqing Boldogh István
Pályázati támogatás:United States National Institute of Environmental Health and Sciences (grant number: RO1 ES018948 to IB)
Egyéb
United States National Institute of Allergic and Infectious Diseases (grant number: PO1-AI062885, to ARB and IB)
Egyéb
United States National Institute of Environmental Health and Sciences Center Grant (grant number: P30 ES006676 to ARB, IB)
Egyéb
National Science Foundation of China (grant number: 31571339 to XB)
Egyéb
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

12.

001-es BibID:BIBFORM114251
035-os BibID:(scopus)85168388624 (wos)001050570800001 (cikkazonosító)1161160
Első szerző:Xue, Yaoyao
Cím:Epigenetic control of type III interferon expression by 8-oxoguanine and its reader 8-oxoguanine DNA glycosylase1 / Xue Yaoyao, Pan Lang, Vlahopoulos Spiros, Wang Ke, Zheng Xu, Radak Zsolt, Bacsi Attila, Tanner Lloyd, Brasier Allan R., Ba Xueqing, Boldogh Istvan
Dátum:2023
ISSN:1664-3224
Megjegyzések:Interferons (IFNs) are secreted cytokines with the ability to activate expression of IFN stimulated genes that increase resistance of cells to virus infections. Activated transcription factors in conjunction with chromatin remodelers induce epigenetic changes that reprogram IFN responses. Unexpectedly, 8-oxoguanine DNA glycosylase1 (Ogg1) knockout mice show enhanced stimuli-driven IFN expression that confers increased resistance to viral and bacterial infections and allergen challenges. Here, we tested the hypothesis that the DNA repair protein OGG1 recognizes 8-oxoguanine (8-oxoGua) in promoters modulating IFN expression. We found that functional inhibition, genetic ablation, and inactivation by post-translational modification of OGG1 significantly augment IFN-? expression in epithelial cells infected by human respiratory syncytial virus (RSV). Mechanistically, OGG1 bound to 8-oxoGua in proximity to interferon response elements, which inhibits the IRF3/IRF7 and NF-?B/RelA DNA occupancy, while promoting the suppressor NF-?B1/p50-p50 homodimer binding to the IFN-?2/3 promoter. In a mouse model of bronchiolitis induced by RSV infection, functional ablation of OGG1 by a small molecule inhibitor (TH5487) enhances IFN-? production, decreases immunopathology, neutrophilia, and confers antiviral protection. These findings suggest that the ROS-generated epigenetic mark 8-oxoGua via its reader OGG1 serves as a homeostatic thresholding factor in IFN-? expression. Pharmaceutical targeting of OGG1 activity may have clinical utility in modulating antiviral response.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Frontiers in Immunology. - 14 (2023), p. 1-19. -
További szerzők:Pan, Lang Vlahopoulos, Spiros A. Wang, Ke Zheng, Xu Radák Zsolt Bácsi Attila (1967-) (immunológus) Tanner, Lloyd Brasier, Allan R. Ba, Xueqing Boldogh István
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1 
Corvina könyvtári katalógus v8.2.27 © 2023 Monguz kft. Minden jog fenntartva.