NDLI: Innate Inflammation Induced by the 8-Oxoguanine DNA Glycosylase-1-KRAS-NF-κB Pathway

Content Provider	PubMed Central
Author	Leopoldo, Aguilera-aguirre Bacsi, Attila Zsolt, Radak Hazra, Tapas K. Mitra, Sankar Sur, Sanjiv Brasier, Allan R. Ba, Xueqing Istvan, Boldogh
Abstract	8-Oxoguanine-DNA glycosylase-1 (OGG1) is the primary enzyme for repairing 7,8-dihydro-8-oxoguanine (8-oxoG) via the DNA base 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. Here we proposed that the mechanistic link between OGG1-BER and pro-inflammatory gene expression is OGG1’s guanine nucleotide exchange factor activity, acquired after release of the 8-oxoG base and consequent activation of the small GTPase RAS. To test this hypothesis, we utilized BALB/c mice expressing or deficient in OGG1 in their airway epithelium and various molecular biological approaches, including active RAS pull-down, reporter and Comet assays, siRNA-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-, PI3-, and MS kinases for NF-κB activation, pro-inflammatory chemokine/cytokine expression, and inflammatory cell recruitment to the airways. Mice deficient in OGG1-BER showed significantly decreased immune responses, while 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.
Related Links	http://dx.doi.org/10.4049/jimmunol.1401625
Ending Page	4653
Page Count	11
Starting Page	4643
File Format	PDF
ISSN	15506606
e-ISSN	15506606
Journal	Journal of immunology (Baltimore, Md. : 1950)
Issue Number	9
Volume Number	193
Language	English
Publisher Date	2014-11-01
Access Restriction	Open
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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