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KLF13 promotes SLE Pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes [RNA-seq]

ABSTRACT: KLF13 promotes SLE Pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes [RNA-seq]

PROVIDER: PRJNA1165281 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30799040.fastq.gz	Fastqsanger.gz
	SRR30799041.fastq.gz	Fastqsanger.gz
	SRR30799042.fastq.gz	Fastqsanger.gz
	SRR30799043.fastq.gz	Fastqsanger.gz
	SRR30799044.fastq.gz	Fastqsanger.gz

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KLF13 promotes SLE Pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes

Project description:KLF13 promotes SLE Pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes

| PRJNA1165278 | ENA

KLF13 promotes SLE Pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes [RNA-seq]

Project description:Although significant progress has been achieved in elucidating the genetic architecture of systemic lupus erythematosus (SLE), identifying genes underlying the pathogenesis has been challenging. The NZM2410-derived lupus susceptibility Sle3 locus is associated with T cell hyperactivity and activated myeloid cells. However, candidate genes associated with these phenotypes have not been identified. Here, we narrow the Sle3 locus to a smaller genomic segment (Sle3k) and show that mice carrying Sle3k and Sle1 loci developed lupus nephritis. We identify Klf13 as the primary candidate gene upregulated in Sle3k mice and demonstrate that Klf13 upregulation is associated with genome-wide transcription changes resulting in higher levels of proinflammatory cytokines, enhanced T cell activation, and hyperresponsiveness of myeloid cells. Correspondingly, Klf13 –/– mice display striking repression of genes involved in mediating immune activation, including key proinflammatory cytokines/chemokines. Furthermore, Klf13 –/– mice show profound dysregulation in cytokine signaling pathways in myeloid cells in response to toll receptor ligands, thus revealing a key role of KLF13 in modulating myeloid cell function. Klf13 upregulation is associated with increased production of RANTES, a key chemokine in lupus nephritis, in activated T cells and the kidneys of lupus-prone mice. In sum, our findings reveal Klf13 as a key gene in the Sle3 interval in mediating lupus pathogenesis that may have implications in the rational design of new therapies for SLE and other autoimmune/inflammatory diseases.

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KLF13 promotes SLE Pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes [ATAC-seq]

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KLF13 promotes SLE Pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes [ATAC-seq]

Project description:KLF13 promotes SLE Pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes [ATAC-seq]

| PRJNA1165276 | ENA

KLF13 promotes SLE Pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes

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

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Nrf2 suppresses macrophage inflammatory response by blocking proinflammatory cytokine transcription

Project description:Nrf2 (NF-E2-related factor-2) transcription factor regulates oxidative/xenobiotic stress response and also represses inflammation. However, the mechanisms how Nrf2 alleviates inflammation are still unclear. Here, we demonstrate that Nrf2 interferes with lipopolysaccharide-induced transcriptional upregulation of proinflammatory cytokines, including IL-6 and IL-1Î². ChIP-seq and ChIP-qPCR analyses revealed that Nrf2 binds to the proximity of these genes in macrophages and inhibits RNA Pol II recruitment. Further, we found that Nrf2-mediated inhibition is independent of the Nrf2 binding motif and reactive oxygen species level. Murine inflammatory models further demonstrated that Nrf2 interferes with IL6 induction and inflammatory phenotypes in vivo. Thus, contrary to the widely accepted view that Nrf2 suppresses inflammation through redox control, we demonstrate here that Nrf2 opposes transcriptional upregulation of proinflammatory cytokine genes. This study identifies Nrf2 as the upstream regulator of cytokine production and establishes a molecular basis for an Nrf2-mediated anti-inflammation approach. Gene expression in BMDMs obtained from wild-type and Keap1-CKO mice. In Keap1-CKO (Keap1 flox/flox::LysM-Cre) BMDMs, Nrf2 transcription factor is activated due to Keap1-deficiency. BMDMs were obtained by a culture of bone marrow cells in the presence of M-CSF for7 days. M1-activated BMDMs were obtained by stimulation with LPS and IFNg for 6 hours, while M2-activated BMDMs were obtained by a stimulation with IL-4 for 6 hours. Two independent BMDM cultures were performed, and each experiment contains samples obtained from one wild-type and one Keap1-CKO mice, respectively.

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Nrf2 suppresses macrophage inflammatory response by blocking proinflammatory cytokine transcription

2016-05-12 | GSE71263 | GEO

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