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A20 attenuate oxidized self-DNA mediated inflammasome activation in AKI [AA-DNA]

ABSTRACT: To seek out the target of restricting the exaggerated inflammation results from ox-self-DNA, we treated BMDMs with self-dsDNA from kidney of acute kidney injury mice model. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different groups of BMDMs.

ORGANISM(S): Mus musculus

PROVIDER: GSE219187 | GEO | 2022/12/20

REPOSITORIES: GEO

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A20 attenuate oxidized self-DNA mediated inflammasome activation through promoting NEK7 ubiquitination in AKI [ox-dsDNA90]

Project description:To seek out the target of restricting the exaggerated inflammation results from ox-dsDNA90, we treated BMDMs with ox-dsDNA90 from kidney of acute kidney injury mice model. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different groups of BMDMs.

2022-12-20 | GSE219188 | GEO

A20 attenuate oxidized self-DNA mediated inflammasome activation in AKI [AA-DNA]

Project description:A20 attenuate oxidized self-DNA mediated inflammasome activation in AKI [AA-DNA]

| PRJNA907368 | ENA

A20 attenuate oxidized self-DNA mediated inflammasome activation through promoting NEK7 ubiquitination in AKI [ox-dsDNA90]

Project description:A20 attenuate oxidized self-DNA mediated inflammasome activation through promoting NEK7 ubiquitination in AKI [ox-dsDNA90]

| PRJNA907369 | ENA

A20 attenuate oxidized self-DNA mediated inflammasome activation through promoting NEK7 ubiquitination in AKI

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-12-20 | GSE219189 | GEO

A20 attenuate oxidized self-DNA mediated inflammasome activation through promoting NEK7 ubiquitination in AKI

Project description:A20 attenuate oxidized self-DNA mediated inflammasome activation through promoting NEK7 ubiquitination in AKI

| PRJNA907366 | ENA

Oxidized mitochondrial DNA sensing by plasmacytoid dendritic cells bypasses self-tolerance to trigger Tfh dependent autoantibody production [scRNA-seq]

Project description:Damage associated molecular patterns (DAMP) trigger inflammation and provide co-stimulatory signals to adaptive immune cells, but whether and how recurring innate stimuli circumvent self-tolerance and initiate maladaptive autoimmunity is unknown. We explored if oxidized mitochondrial DNA (Ox-mtDNA), a DAMP released by stressed macrophages, found in higher amounts in diverse metabolic and autoimmune disorders, including systemic lupus erythematosus (SLE), initiates antibody-mediated autoimmunity. Indeed, Ox-mtDNA release induced by repetitive alum challenges elicited germinal center reactions, autoantibody production and nephropathology. These responses were recapitulated by in-vitro generated Ox-mtDNA, while non-oxidized mtDNA was non-pathogenic. Both mtDNA forms, but not nuclear DNA, were internalized by plasmacytoid dendritic cells (pDC), activated NF-kB via TLR9 and induced interferon (IFN)-I. Yet only Ox-mtDNA triggered NLRP3- and gasdermin D-dependent IL-1β secretion, eliciting autocrine production of IL-21 that together with IL-1β, but independently of IFN-I, enabled pDC to convert naïve CD4+ T cells into follicular helper cells. Highlighting Ox-mtDNA as a uniquely immunogenic DAMP that is specifically sensed by pDC and IL-1β as an orchestrator of autoantibody production, these findings explain how chronic inflammation culminates in autoimmunity and unravel new therapeutic targets applicable to SLE, the autoimmune/inflammatory syndrome induced by adjuvants (ASIA) and related diseases.

2025-04-10 | GSE264620 | GEO

Oxidized mitochondrial DNA sensing by plasmacytoid dendritic cells bypasses self-tolerance to trigger Tfh dependent autoantibody production [RNA-seq]

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Identification of oxidized cysteine residues in signaling proteins in U937 cells at basal levels and upon diamide and hypochlorous acid stimulations.

Project description:Here, we report a detection of oxidative post-translational modifications (ox-PTM) of Cys residues in the U937 cell line either non-stimulated or stimulated with diamide, a thiol-oxidizing agent at 0.5mM for 20min or HOCl at 100µM for 10min. Reversible Cys ox-PTMs were labelled using a bioswitch method using a Maleimide-(Polyethylene Glycol)2-Biotin (Mal-PEG2-Bio) probe independently of the oxidation type. Labeled proteins were analyzed by Mass spectrometry. We identified Cys ox-PTMs encompassing 1473 proteins containing at least ox-PTM-modified Cys. These sites include ox-PTM sites previously described in vitro validating the approach. Numerous novel Cys susceptible to ox-PTMs were identified including signaling proteins, including kinases, phosphatases and transcription and translation factors and proteins relevant to virus-host interactions.

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Unique Transcriptional Programs Identify Subtypes of AKI

Project description:Two metrics, a rise in serum creatinine concentration and a decrease in urine output, are considered tantamount to the injury of the kidney tubule and the epithelial cells thereof (AKI).Yet neither criterion emphasizes the etiology or the pathogenetic heterogeneity of acute decreases in kidney excretory function. In fact, whether decreased excretory function due to contraction of the extracellular fluid volume (vAKI) or due to intrinsic kidney injury (iAKI) actually share pathogenesis and should be aggregated in the same diagnostic group remains an open question. To examine this possibility, we created mouse models of iAKI and vAKI that induced a similar increase in serum creatinine concentration. Using laser microdissection to isolate specific domains of the kidney, followed by RNA sequencing, we found that thousands of genes responded specifically to iAKI or to vAKI, but very few responded to both stimuli. In fact, the activated gene sets comprised different, functionally unrelated signal transduction pathways and were expressed in different regions of the kidney. Moreover, we identified distinctive gene expression patterns in human urine as potential biomarkers of either iAKI or vAKI, but not both. Hence, iAKI and vAKI are biologically unrelated, suggesting that molecular analysis should clarify our current definitions of acute changes in kidney excretory function.

2016-12-01 | GSE81741 | GEO

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