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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE169052 | GEO | 2021/03/17

REPOSITORIES: GEO

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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

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

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

| PRJNA714967 | ENA

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

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 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

Downregulation of Sox8 mediates monosodium urate crystal-induced autophagic impairment of cartilage in gout arthritis.

Project description:The deposition of monosodium urate (MSU) crystals in arthritic joints of gout seriously damages cartilage. This study aimed to investigate whether MSU crystal-induced cartilage impairment was related to autophagic signaling. mRNAs of cartilage from MSU-induced gouty arthritis rat model were sequenced. MSU crystal-treated human chondrocytes were used to evaluate the function of Sox8. The recombinant Sox8 lentiviral vector (lenti-Sox8) was applied to upregulate the expression of Sox8. Transfection of the mRFP-GFP-LC3 plasmid was evaluated by confocal microscopy. The autophagic vacuoles were stained with monodansylcadaverine and examined by flow cytometry. The morphology of autophagosomes was observed by transmission electron microscopy. The ratio of LC3-II/I in the presence or absence of bafilomycin A1 and the expression levels of Beclin1, Sox8, p-PI3K, PI3K, p-AKT, AKT, p-mTOR, and mTOR were detected by Western blot. In vivo, the effect of Sox8 on cartilage of acute gouty model rats was evaluated by safranin-O/fast green staining and Western blot. The expression of Sox8 was significantly downregulated both in vivo and in vitro. In chondrocytes, MSU crystals reduced the expression of Sox8, inhibited the PI3K/AKT/mTOR signaling pathway, and increased the level of autophagy. Overexpression of Sox8 notably inhibited MSU crystal-induced autophagy by rescuing the phosphorylation levels in the PI3K/AKT/mTOR signaling pathway. In vivo, overexpression of Sox8 remarkably alleviated cartilage damage in acute gouty model rats. These results indicate that downregulation of Sox8 plays an important role in MSU-induced chondrocyte autophagy by modulating PI3K/AKT/mTOR signaling, and overexpression of Sox8 may serve as a novel therapy to prevent the impairment of cartilage in gout arthritis.

| S-EPMC10015026 | biostudies-literature

Monosodium urate-crystal-stimulated phospholipase D in human neutrophils.

Project description:Protein kinase Calpha (PKCalpha) and small GTPases of the Rho and ADP-ribosylation factor (Arf) family are implicated in the regulation of phospholipase D1 (PLD1) activity. Although they are involved in fMet-Leu-Phe (fMLP)-mediated PLD activation, their role in monosodium urate (MSU)-stimulated PLD1 activity in human neutrophils is not clear. The translocation of PKCalpha, RhoA and Arf from the cytosol to the membranes was monitored. fMLP induced a cytochalasin B (CB)-dependent recruitment of Arf, RhoA and PKCalpha to neutrophil membranes. CB also increased the activation of PLD 10-fold. In contrast with fMLP, MSU stimulated a sustained and time-dependent relocalization of Arf and PKCalpha, but not of RhoA, to the membrane fraction. MSU-stimulated PLD was activated with a time course preceding membrane recruitment of Arf and PKCalpha in the absence of CB. Furthermore, MSU-induced PLD activation and the membrane recruitment of PKCalpha, but not that of Arf, were inhibited by CB. An anti-FcgammaRIIIB antibody, VIFcRIII, prevented the membrane relocalization of Arf and PKCalpha and the stimulation of the levels of tyrosine phosphorylation and of PLD activity induced by MSU. Erbstatin and ST-638, two inhibitors of tyrosine kinases, inhibited the MSU-induced translocation of Arf and PKCalpha but not MSU-induced tyrosine phosphorylation and PLD activation. Furthermore MSU crystals did not cause the tyrosine phosphorylation of PLD1. The present study indicates that soluble and particulate agonists show selectivity in inducing the translocation of RhoA in neutrophils and that the ability of MSU to increase PLD activation was independent of the membrane relocalization of Arf and PKCalpha.

| S-EPMC1219951 | biostudies-other

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