Ontology highlight
ABSTRACT:
PROVIDER: PRJNA893078 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22012222.fastq.gz | Fastqsanger.gz | |||
| SRR22012223.fastq.gz | Fastqsanger.gz | |||
| SRR22012224.fastq.gz | Fastqsanger.gz | |||
| SRR22012225.fastq.gz | Fastqsanger.gz | |||
| SRR22012226.fastq.gz | Fastqsanger.gz |
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Project description:As a prominent feature of gout, monosodium urate (MSU) crystal deposition can induce gout flare, yet its impact on blood immune in gout remission patients still remains unclear. In this study, single-cell RNA sequencing (scRNA-seq) is used to compare the gene expression profiling of peripheral blood mononuclear cells (PBMCs) among intercritical gout remission patients, advanced gout remission patients and healthy volunteers. The increase of HLA-DQA1high classical monocytes, and their important role in immune inflammatory responses and osteoclast differentiation are discovered in advanced gout remission patients. Moreover, the differentiation level of CD8+T cells are found to elevate in advanced gout remission patients, which is further validated via flow cytometry. It is also observed that pathways related to bone metabolism and inflammatory responses are overactive in advanced gout remission patients. By analysis on intercellular communication network, immune-related cell-cell interactions among PBMCs are shown to enhance in both intercritical and advanced gout remission patients. The analyses on gene expression and LC-MS/MS together indicate the increased metabolic level of arachidonic acid in gout remission patients with MSU deposition at the intercritical and advanced stage. The study reveals distinctive blood immune characteristics in gout remission with MSU deposition, which provides more sights into its pathogenesis.
2023-06-01 | GSE217561 | GEO
Project description:Gout is a common inflammatory arthritis caused by precipitation of monosodium urate (MSU) crystals in individuals with hyperuricemia. Acute flares are accompanied by secretion of pro-inflammatory cytokines, including interleukin-1 beta (IL-1B). Clonal hematopoiesis of indeterminate potential (CHIP) is an age-related condition predisposing to hematologic cancers and cardiovascular disease. CHIP is associated with elevated IL-1B, thus we investigated CHIP as a risk factor for gout. To test the clinical association between CHIP and gout, we analyzed whole exome sequencing data from 177,824 individuals in the MGB Biobank (MGBB) and UK Biobank (UKB). In both cohorts, the frequency of gout was higher among individuals with CHIP than without CHIP (MGBB, CHIP with variant allele fraction [VAF] ≥2%: OR, 1.69; 95% CI, 1.09-2.61; P=0.0189; UKB, CHIP with VAF ≥10%: OR, 1.25; 95% CI, 1.05-1.50; P=0.0133). Moreover, individuals with CHIP and a VAF ≥10% had an increased risk of incident gout (UKB: HR, 1.28; 95% CI, 1.06-1.55; P=0.0107). In murine models of gout pathogenesis, animals with Tet2 knockout hematopoietic cells had exaggerated IL-1B secretion and paw edema upon administration of MSU crystals. Tet2 knockout macrophages elaborated higher levels of IL-1B in response to MSU crystals in vitro, and this was ameliorated through genetic and pharmacologic Nlrp3 inflammasome inhibition. These studies show that TET2-mutant CHIP is associated with an increased risk of gout in humans and that MSU crystals lead to elevated IL-1B levels in Tet2 knockout murine models. We identify CHIP as an amplifier of NLRP3-dependent inflammatory responses to MSU crystals in gout patients.
2022-06-14 | GSE205963 | GEO
Project description:Gout is a prevalent and painful inflammatory arthritis, and its global burden continues to rise. Intense pain induced by gout attacks is a major complication of gout. Treatment and long-term management for gout patients remain challenging. Despite the discovery of many key immune response and inflammatory genes and pathways in gout, the molecular mechanisms of gout inflammation are still not entirely elucidated. Particularly, systematic studies of gout inflammation and pain are lacking. Using a monosodium urate (MSU) crystals-induced gout model, we performed genome-wide transcriptome analysis for the ankle joint, dorsal root ganglion (DRG), and spinal cord of gout mice. Our results revealed transcriptional changes in both the joint and the nervous system. Furthermore, through integrated analysis with public datasets of mouse inflammatory pain and neuropathic pain models, human GWAS, osteoarthritis (OA), and rheumatoid arthritis (RA), we identified common and unique features associated with acute gout inflammation and severe pain.
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Project description:Objectives: In gout, flares of severely painful inflammatory arthritis intersect with metabolism, circadian rhythm, and macrophage activation. NAD+ is a necessary cofactor and key metabolite in cellular bioenergy homeostasis, and NAD+ suppresses the NLRP3 inflammasome and inflammation. However, cellular NAD+ declines in inflammatory states, associated with increased activity of the leukocyte-expressed NADase CD38. Gouty arthritis is principally prevented and treated with nonselective and frequently toxic drugs (colchicine, NSAIDs, corticosteroids). Hence, we tested the potential role of therapeutically targeting CD38 and NAD+ in gout. Methods: We studied cultured mouse wild type and CD38 knockout (KO) murine bone marrow derived macrophages (BMDMs) stimulated by monosodium urate (MSU) crystals, and the air pouch gout synovitis model. Results: MSU crystals induced CD38 in BMDMs in vitro, associated with NAD+ depletion, and IL-1b and CXCL1 release, effects reversed by pharmacologic CD38 inhibitors (apigenin, 78c). Mouse air pouch inflammatory responses to MSU crystals were blunted by CD38 KO and apigenin. Pharmacologic CD38 inhibition suppressed MSU crystal-induced NLRP3 inflammasome activation and increased anti-inflammatory SIRT3-SOD2 in macrophages. BMDM RNA-seq analysis of 176 differentially expressed genes (DEGs) revealed CD38 control of multiple MSU crystal-modulated inflammation pathways. The top DEGs included the circadian rhythm modulator GRP176, and the metalloreductase STEAP4 that mediates iron homeostasis, and promotes oxidative stress and NF-kB activation when it is overexpressed. Conclusion: CD38 and NAD+ depletion are druggable targets controlling the MSU crystal- induced inflammation program. Targeting CD38 and NAD+ are potentially novel selective molecular approaches to limit gouty arthritis.
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Project description:Gout arthritis (GA) is a prevalent and painful inflammatory arthritis, and its global burden continues to rise. Intense pain induced by gout attacks is a major complication of gout. Treatment and long-term management for gout patients remain challenging. However, the pathogenesis of GA still remained largely unknown. The purpose of this study is to perform an expression profiling to identify genes related with GA in an animal model. Using a monosodium urate (MSU) crystals-induced GA model, we performed RNA-sequencing for the ankle joint of gout mice in different time points. Our results revealed transcriptional changes in the joint. We provided by far the first study to profile gene expression changes and pathway analysis of ankle joint in different time for investigating GA mechanisms. This work may provide novel insights into understanding the mysterious mechanisms underlying GA.
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Project description:To determine the expression profile and clinical significance of circular RNAs (circRNAs) in peripheral blood mononuclear cells (PBMCs) of patients with primary gout and healthy control subjects. Human circRNA microarrays were used to identify the differentially expressed circRNAs in primary gout (Gout, n = 5) and healthy subjects (HC, n = 3). Bioinformatics analyses were performed to predict the roles of differently expressed circRNAs. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to validate the results in 90 gout patients, and 60 healthy control subjects (HC). Microarray analysis indicated that 238 circRNAs were up-regulated and 41 circRNAs were down-regulated in the Gout group (Fold change>1.5, p-value<0.05). Bioinformatics analysis showed that differentially expressed circRNAs were involved in the pathogenesis of gout through a variety of different pathways. Significant association was observed between these circRNAs and lipid metabolism indicators. Our results provide novel insight into the mechanisms of primary gout, and reveal that hsa_circRNA_103657 could effectively discriminate the gout group and the healthy control groups.
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Project description:To determine the expression profile and clinical significance of long non-coding RNAs (lncRNAs) in peripheral blood mononuclear cells (PBMCs) of patients with primary gout and healthy control subjects. Human lncRNA microarrays were used to identify the differentially expressed lncRNAs and mRNAs in primary gout (n=6) and healthy subjects (n=6). Bioinformatics analyses were performed to predict the roles of differently expressed lncRNAs and mRNAs. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to validate the results in 64 gout patients, and 32 healthy control subjects (HC). The microarray analysis identified 1479 differentially expressed lncRNAs (879 up-regulated and 600 down-regulated), 862 differentially expressed mRNAs (390 up-regulated and 472 down-regulated) in primary gout (fold change>2, P<0.05), respectively. The bioinformatic analysis indicated that the differentially expressed lncRNAs regulated the abnormally expressed mRNAs, which were involved in the pathogenesis of gout through several different pathways. Significant association was observed between these lncRNAs and the Clinical inflammation indicators and lipid metabolism indicators. Our results provide novel insight into the mechanisms of primary gout, and reveal that ENST00000566457 and NR-026756 could effectively discriminate the gout group and the healthy control groups.
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