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Epigenetic regulator UHRF1 suppressively organize multiple pathogenesis in rheumatoid arthritis [MBD-seq]

ABSTRACT: Epigenetic regulator UHRF1 suppressively organize multiple pathogenesis in rheumatoid arthritis [MBD-seq]

PROVIDER: PRJNA701904 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13711236_1.fastq.gz	Fastqsanger.gz
	SRR13711236_2.fastq.gz	Fastqsanger.gz
	SRR13711237_1.fastq.gz	Fastqsanger.gz
	SRR13711237_2.fastq.gz	Fastqsanger.gz
	SRR13711238_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Epigenetic regulator UHRF1 suppressively organize multiple pathogenesis in rheumatoid arthritis [MBD-seq]

Project description:Rheumatoid arthritis (RA) is characterized by chronic synovial inflammation with aberrant epigenetic alterations, leading joint destruction. However, epigenetic regulatory mechanisms underlying RA pathogenesis remain largely unknown. Here we showed that Ubiquitin-like containing PHD and RING finger domains 1 (known as UHRF1) is a central epigenetic regulator to suppressively orchestrate the expression of multiple exacerbation factors in RA. We found remarkable up-regulation of Uhrf1, which is known as a key molecular for maintenance of DNA methylation during cell division 1-3, in murine arthritis tissue, especially synovial fibroblasts (SF). SF-specific Uhrf1 conditional knockout mice indicated more severe arthritic phenotypes with apoptosis resistant SF. Integrative analysis between transcriptome and methylome showed that expression of several cytokines including Ccl20 were up-regulated in Uhrf1-deficient SF. In RA patients, disease activity scores, CCL20 expression, Th17 accumulation, apoptosis resistance were negatively correlated with UHRF1 expression in synovium. Finally, stabilization of UHRF1 by administration of Ryuvidine improved pathogenesis of arthritis model mice. Our results demonstrated that UHRF1 expressed in SF contributes to suppressively orchestrate expression of genes of multiple exacerbating factors under RA progression. Targeting UHRF1 could provide a novel therapeutic strategy for RA.

2021-02-16 | GSE166747 | GEO

Epigenetic regulator UHRF1 suppressively organize multiple pathogenesis in rheumatoid arthritis.

Project description:Epigenetic regulator UHRF1 suppressively organize multiple pathogenesis in rheumatoid arthritis.

| PRJNA701897 | ENA

Epigenetic regulator UHRF1 suppressively organize multiple pathogenesis in rheumatoid arthritis [RNA-seq]

2021-02-16 | GSE166746 | GEO

Epigenetic regulator UHRF1 suppressively organize multiple pathogenesis in rheumatoid arthritis [RNA-seq]

Project description:Epigenetic regulator UHRF1 suppressively organize multiple pathogenesis in rheumatoid arthritis [RNA-seq]

| PRJNA701902 | ENA

Epigenetic regulator UHRF1 suppressively organize multiple pathogenesis in rheumatoid arthritis.

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

2021-02-16 | GSE166748 | GEO

Uhrf1 control the proliferation and the differentiation of satellite cells [MBD-seq]

Project description:Uhrf1 control the proliferation and the differentiation of satellite cells [MBD-seq]

| PRJNA715492 | ENA

Rheumatoid arthritis

Project description:Rheumatoid arthritis (RA) is a chronic, inflammatory joint disease of unknown etiology and pronounced inter-patient heterogeneity. To characterize RA at the molecular level and to uncover key pathomechanisms, we performed whole-genome gene expression analyses. Synovial tissues from rheumatoid arthritis patients were compared to those from osteoarthritis patients and to normal donors. Keywords: disease state analysis

2004-11-04 | GSE1919 | GEO

Uhrf1 control the proliferation and the differentiation of satellite cells [MBD-seq]

Project description:DNA methylation is an essential epigenetic regulation for cellular identity. In muscle stem cells, termed satellite cells, DNA methylation patterns are dynamically changed during muscle regeneration. However, how these DNA methylation patterns are maintained remain unclear. Here, we demonstrate that a key epigenetic regulator Uhrf1 (ubiquitin-like with PHD and RING finger domains 1) is activated in proliferating but not expressed in quiescent or differentiated satellite cells. Ablation of Uhrf1 in satellite cell impairs the proliferation and differentiation of satellite cells, leading to failure of muscle regeneration. Loss of Uhrf1 in satellite cells alters transcriptional programs and leads to DNA hypomethylation with the activation of Cdkn1a and Notch signalling. Down-regulation of Cdkn1a and Notch signalling rescued the proliferation and differentiation defect in Uhrf1-deficient satellite cells. Therefore, this study suggest that Uhrf1 can regulate the self-renewal and differentiation of satellite cells through DNA methylation patterning.

2022-02-04 | GSE169184 | GEO

Rheumatoid arthritis: aortic biopsies

Project description:Rheumatoid arthritis: aortic biopsies

| PRJNA432552 | ENA

Differential DNA methylation in Rheumatoid arthritis

Project description:Genome-wide DNA methylation level was studied to determine whether Rheumatoid arthritis patients (cases) has methylation differences comparing to normal controls in PBLs. We used Illumina HumanMethylation450 BeadChip array to determine the genome-wide DNA methylation difference in PBLs from Rheumatoid arthritis patients (cases) and normal controls Bisulphite converted DNA from the Rheumatoid arthritis patients (cases) and normal controls were hybridized to the Illumina Illumina HumanMethylation450 BeadChip arrays

2013-01-21 | E-GEOD-42861 | biostudies-arrayexpress

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