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Transcriptomic analysis of primed synovial fibroblasts from monosodium urate crystal-induced arthritis in the mouse [RNA-seq]

ABSTRACT: Transcriptomic analysis of primed synovial fibroblasts from monosodium urate crystal-induced arthritis in the mouse [RNA-seq]

PROVIDER: PRJNA714967 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13981720.fastq.gz	Fastqsanger.gz
	SRR13981721.fastq.gz	Fastqsanger.gz
	SRR13981722.fastq.gz	Fastqsanger.gz
	SRR13981723.fastq.gz	Fastqsanger.gz
	SRR13981724.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of primed synovial fibroblasts from monosodium urate crystal-induced arthritis in the mouse

Project description:Transcriptomic analysis of primed synovial fibroblasts from monosodium urate crystal-induced arthritis in the mouse

| PRJNA714965 | ENA

Transcriptomic analysis of synovial fibroblasts from monosodium urate crystal-induced arthritis with or without I-BET151 treatment.

Project description:We used I-BET 151, an isoxazoloquinoline that specifically inhibits interaction of BET proteins with acetylated histones to restrict inflammatory tissue priming in a mouse model of iterated monosodium urate (MSU) crystal-induced arthritis. Systemic administration of I-BET 151 abolished the enhancement of arthritis upon repeated injection of MSU crystals.

2022-02-17 | GSE196679 | GEO

Transcriptomic analysis of cultured primed synovial fibroblasts from monosodium urate crystal-induced arthritis in the mouse (validation set of samples)

Project description:Transcriptomic analysis of cultured primed synovial fibroblasts from monosodium urate crystal-induced arthritis in the mouse (validation set of samples)

| PRJNA687412 | ENA

Transcriptomic analysis of primed synovial fibroblasts from monosodium urate crystal-induced arthritis in the mouse [RNA-seq]

Project description:Repeated challenge of synovial fibroblasts with MSU crystals in vivo induced inflammatory priming.

2021-03-17 | GSE169050 | GEO

Study of transcriptional effects of monosodium urate crystal (MSU) on HaCaT keratinocyte cell line.

2015-10-29 | GSE65931 | GEO

Transcriptomic analysis of cultured primed synovial fibroblasts from monosodium urate crystal-induced arthritis in the mouse (validation set of samples)

Project description:Repeated challenge of synovial fibroblasts with MSU crystals in vivo induced inflammatory priming

2020-12-24 | GSE163749 | GEO

Transcriptomic analysis of synovial fibroblasts from monosodium urate crystal-induced arthritis with or without I-BET151 treatment.

Project description:Transcriptomic analysis of synovial fibroblasts from monosodium urate crystal-induced arthritis with or without I-BET151 treatment.

| PRJNA806842 | ENA

Lymphatic vessels drain monosodium urate and activate immunity in gouty arthritis

Project description:Gouty Arthritis (GA) is caused by urate deposition in the joint capsule, cartilage, bone, and surrounding tissues to trigger recurrent attacks of acute joint inflammation. However, the clearance mechanism of urate deposition is still not clear. We aimed to investigate whether lymphatics vessels can drain monosodium and involve in the immune process of GA. Methods: Inguinal lymph nodes (LNs) in 4 normal volunteers and 4 patients with acute flare of GA were examined by ultrasound. Acute and chronic GA flare mouse models were established by intra-footpad administrations of monosodium urate (MSU) for 1 week or 1 month. Mice were treated with VEGFR-3 inhibitor or undergone popliteal lymph node (PLN) excision or PLN macrophage depletion. The severity of foot inflammation, lymphatic draining function, concentration of uric acid (UA), and macrophage population were examined. Macrophages were co-cultured with MSU-treated lymphatic endothelial cells (LECs) and differential gene expression of LECs was assessed by Agilent gene expression microarray. Results: 1) Draining LNs were enlarged in patients with GA flare and GA mouse models. 2) The lymphatic function and structure were abnormal in GA mouse models. 3) Acute GA mice had elevated UA levels in draining LNs, but not in the serum, while chronic GA mice had elevated UA levels in both LNs and serum. 4) Blockade of VEGFR-3 reduced foot inflammation in chronic GA mice. 5) MSU induces pro-inflammatory polarization of macrophages by inducing LEC inflammation. 6) PLN local depletion of macrophages or removal of PLNs alleviated foot inflammation in GA. Conclusions: Lymphatics drain MSU to the draining LNs to clear deposited urate in the distal extremity and induce LECs to stimulate macrophage pro-inflammatory response during GA. We have identified a novel mechanism about MSU clearance and pro-inflammatory macrophage activation, and provided possible therapeutic approach for GA.

2022-04-02 | GSE199950 | GEO

Study of transcriptional effects of monosodium urate crystal (MSU) on HaCaT keratinocyte cell line.

Project description:Aim of the study was to characterize at a molecular level (changes in transcriptomes) the effect of monosodium urate crystal (MSU) on HaCaT keratinocyte cell line. This was adressed by using a culture model. The HaCaT cell line (human keratinocytes) was stimulated by MSU (1mg/mL) vs control for 12 hrs. By using genome-wide expression profiling, we identified deregulation of functionally relevant gene networks. HaCaT were obtained from Cell Lines Service (Eppelheim, Germany) and grown in DMEM medium (PAN biotech, Aidenbach, Germany) supplemented with 10% FBS (Life Technology, Grand Island, NY, USA), L-glutamine and non-essential amino acid. Before the treatment HaCaT cells were cultured in serum-free medium for 12hrs. HaCaT were treated with MSU (1mg/ml) vs DMEM control for 12hrs then submitted to RNA extration and gene expression profiling. Triplicate experiments were performed: HaCaT control (n=3), MSU-treated (n=3).

2015-10-29 | E-GEOD-65931 | biostudies-arrayexpress

Identification of novel monosodium urate crystal-induced mRNAs

Project description:Objective. To identify novel monosodium urate (MSU) crystal-induced mRNAs by transcript profiling of isolated murine air pouch membranes. Methods. Nine hours after injecting crystals into air pouches, membranes were meticulously dissected away from the adjacent soft tissues. mRNA expression differences between inflamed and control membranes were determined by oligonucleotide microarray analysis. Induction of selected mRNAs was validated by real-time relative quantitative reverse transcriptase PCR (qPCR) in pouch membranes and murine peritoneal macrophages. Results. Eleven of the 12 most highly upregulated mRNAs related to innate immunity and inflammation. They included mRNAs encoding histidine decarboxylase (the enzyme that synthesizes histamine), interleukin (IL)-6, the cell surface receptors PUMA-g and TREM-1, and the polypeptides Irg1 and PROK-2. MSU crystals induced dramatic rises in these mRNAs in the pouch membrane within 3-8 hours after the surge in pro-inflammatory cytokine (IL-6, IL-1beta and TNFalpha) and immediate early gene (Egr-1) transcription, which occurred 1h after crystal injection. MSU crystals induced these mRNAs in cultured macrophages with similar kinetics but lower fold changes. In keeping with their downregulation by MSU crystals according to the microarrays, qPCR confirmed that TREM-2 and granzyme D mRNAs decreased 79% and 94%, respectively, in MSU crystal inflamed membranes. Conclusions. This analysis disclosed several genes previously not implicated in MSU crystal inflammation. Their rise after the early surge in cytokine mRNAs suggests that they may, for instance, amplify or perpetuate inflammation. Transcript profiling of the isolated air pouch membrane promises to be a powerful tool to identify genes acting at different stages of inflammation.

2008-05-23 | GSE11498 | GEO

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