Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

65 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of muscle and liver tissue in collagen-induced arthritis (CIA) and control mice treated with increasing doses of prednisolone

ABSTRACT: Prednisolone is a potent anti-inflammatory glucocorticoid (GC) but chronic use is hampered by metabolic side effects. Although GCs are predominantly prescribed for treatment of inflammatory conditions, little is known about their long-term effects on gene-expression in-vivo during inflammation. Here, we aimed to identify genes underlying prednisolone-induced metabolic side effects in a complex in-vivo inflammatory setting after long-term treatment. We performed whole-genome expression profiling in liver and muscle from arthritic and non-arthritic mice treated with several doses of prednisolone for three weeks.

ORGANISM(S): Mus musculus

SUBMITTER: Sandrine Ellero-Simatos

PROVIDER: E-MTAB-1765 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of DBA/1J mouse with collagen induced arthritis

Project description:Time course of collagen-induced arthritis in DBA/1J male mice, synchronized on day 28 with 10ug LPS

2009-11-16 | E-TABM-661 | biostudies-arrayexpress

Gene expression profile of preclinical arthritis and its modulation by antigen-induced tolerance

Project description:During the course of adjuvant arthritis, maximal changes in gene expression were observed at the incubation phase. A major group of genes affected was related to immune activity. Tolerance induction by mycobacterial heat-shock protein 65 (Bhsp65), the disease-related antigen, caused upregulation of a large number of genes. These included immune activity genes as well as cell proliferation-related genes. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. The draining lymph node cells (LNC) were harvested from arthritic rats at different phases of adjuvant arthritis (incubation,peak and recovery). Also tested were LNC of naïve rats. LNC were tested ex vivo. Total RNA isolated from LNC was used for testing with affymetrix gene chip following manufacturer's instructions. Similarly, LNC of Bhsp65-tolerized rats harvested at incubation phase were tested with or without Bhsp65 restimulation in vitro. LNC of arthritic rats in incubation phase were similarly restimulated with Bhsp65 in vitro as controls, and the results compared with that of the tolerized rats.

2011-11-16 | E-GEOD-31314 | biostudies-arrayexpress

Expression data from footpad of AIRmax and AIRmin mice submitted to pristane arthritis induction

Project description:Mice selected for high and low acute inflammation were tested for pristane induced arthritis, showing to be susceptible and resistant, respectively. We used microarrays to detail the global programme of gene expression underlying arthritis progression during induction and identified distinct classes of differentially expressed genes during this process in the footpad of these mice. AIRmax (high inflammation) and AIRmin (low inflammation) mouse footpads were collected for RNA extraction and hybridization on Affymetrix microarrays. We compared control and experimental footpads from male and female AIRmax and AIRmin mice on days 0 and 160, respectively. Please note that the AIRmax and AIRmin mice were obtained through bidirectional genetic selection, starting with a genetically heterogeneous founder population (F0) produced by intercrossing eight isogenic strains of mice of independent origins (A/J, DBA/2J, P/J, SWR/J, SJL/J, CBA/J, BALB/cJ and C57BL/6J).

2013-10-23 | E-GEOD-51516 | biostudies-arrayexpress

Expression profile of splenocytes with glucose-6-phosphate isomerase (GPI) induced arthritis

Project description:To explore TNF-related genes in GPI-induced arthritis, we performed GeneChip analysis using arthritic splenocytes and control-immunized splenocytes. Among the arrayed TNFalpha-related genes, TIARP mRNA was highly expressed in arthritic splenocytes, with levels exceeding more than 20-times the control splenocytes The spleens of three GPI-GST (MW=89 kD) (300 Âµg) -immunized DBA/1 mice were harvested on day 10. As a control, the spleens of three GST (MW=26 kd) (100 Âµg) -immunized DBA/1 mice were used. Total RNA was extracted from the splenocytes using Isogen (Nippon gene), then 15 ug of RNA was utilized for cDNA synthesis by reverse transcription followed by synthesis of biotinylated cRNA through in vitro transcription. After cRNA fragmentation, hybridization with mouse 430A2.0 GeneChip (Affymetrix, Santa Clara, CA) with probes for 43,000 mouse genes ESTs was performed according to the protocol provided by the manufacturer. Analysis was performed by gene expression software

2010-03-03 | E-GEOD-17272 | biostudies-arrayexpress

Periodontal pathogens do not exacerbate macroscopic arthritis but alter the synovial proteome

Project description:Rheumatoid arthritis (RA) and periodontitis (PD) are chronic inflammatory diseases that appear to occur in tandem. Autoantibodies against citrullinated peptide antigens linked pathogeneses with PD preceding RA. However, the mutual impact PD exerts on RA and vice versa has not yet been defined. To address this issue, we set up an animal model and analyzed how the prime inducers of citrullination - Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans ÃƒÂ¢Ã¢â€šÂ¬Ã¢â‚¬Å“ differ in their pathogenic potential. Our experimental setup included collagen induced arthritis (CIA) in the mouse, oral inoculation with P. gingivalis or A. actinomycetemcomitans to induce alveolar bone loss and the combination of both diseases in inverted orders of events. Label-free quantitative proteome analysis revealed that P. gingivalis and A. actinomycetemcomitans led to differential expression patterns in the synovial membranes that were reminiscent of cellular and humoral immune responses, respectively. The P. gingivalis and A. actinomycetemcomitans specific signatures in the synovial proteomes suggest a role for oral pathogens in shaping disease subtypes and setting the stage for subsequent therapy response.

2020-12-04 | PXD020397 | Pride

Identification of spondylarthropathy-specific genes in BALB/c mice with proteoglycan-induced spondylitis (PGIS)

Project description:BALB/c mice develop peripheral arthritis (PGIA) and spondyloarthropathy (PGIS) upon repeated intraperitoneal injections of human cartilage proteoglycan (PG) aggrecan. The aim of the present study was to identify spondylitis-specific genes by comparing intervertebral disc (IVD) RNA samples from spondyloarthropathic and naM-CM-/ve BALB/c mice. Keywords: Genetic modification We compared the gene expression data of 5 spondyloarthropathic and 3 naM-CM-/ve (control) mice.

2014-04-01 | E-GEOD-13782 | biostudies-arrayexpress

Expression data from mouse arthritis tarsal joints

Project description:Pathological bone changes differ considerably between inflammatory arthritic diseases, and most studies have focused on bone erosion. Collagen Induced Arthritis (CIA) is a model for Rheumatoid Arthritis, which, in addition to bone erosion, demonstrates bone formation at the time for clinical manifestations. The objective of this study was to use the CIA model to study bone remodelling by performing a gene expression profiling time-course study on the CIA model. Three tarsal joints were sampled per clinical phase from the following clinical phases: Duration of clinical arthritis 0-3 days, duration of clinical arthritis 1-2 weeks, duration of clinical arthritis 3-4 weeks and duration of clinical arthritis minimum 3 weeks and declining (Twelve joints in total). For the clinical phase M-bM-^@M-^\DeclineM-bM-^@M-^] the joints had had a clinical score of 3 for minimum 3 weeks, after which the clinical score had declined minimum 1 score when the joint was sampled. For all other joints, the clinical score was 3 at the sampling time. The twelve joints were compared to three joints from non-induced control animals. The joints were processed and analysed separately (unpooledM-BM- ). The joints were snap-frozen in liquid N2 and stored at -80M-KM-^ZC. RNA was extracted using the mirVanaTM miRNA isolation kit (Ambion, Denmark), amplified and labelled using the Pico amplification kit (Nugen, San Carlos, USA), according to the manufacturersM-BM-4 instructions, followed by hybridisation to Mouse Gene 1.0ST microarrays (Affymetrix, Santa Clara, USA). The quality of the RNA was evaluated using RNA integrity numbers (RIN) and only samples with values of minimum 8.4 were chosen for further analysis.

2015-03-01 | E-GEOD-61140 | biostudies-arrayexpress

Transcription profiling of lymph node from mice with collagen induced arthritis in response to the endothelin receptor antagonist Bosentan

Project description:DBA/1J mice (12 wk old; weighing 18-22 g) were housed in temperature-controlled rooms (22-25 C) in the animal facility of the School of Medicine of Ribeir o Preto, University of Sao Paulo, Sao Paulo, Brazil, and received water and food ad libitum. Male DBA/1J mice received 200 g of bovine type II collagen (CII) in CFA by intradermal injection (day 0). Collagen (200 ?g in PBS) was given again on day 21 by i.p. injection. Mice were monitored daily for signs of arthritis for which severity scores were derived as follows: 0=normal, 1=erythema, 2=erythema plus swelling, 3= extension/loss function and total score = sum of four limbs. Disease onset characterized by erythema and/or paw swelling was seen between days 25 and 35. For the therapeutic approach, DBA/1 mice were treated with Bosentan (100 mg kg-1) p.o. or vehicle once a day for a total of 11 days. The treatment began on day that CIA became clinically detectable. The DBA-1/J mice were sacrificed preferentially by CO2 inhalation, and the lymph nodes removed. To obtain sufficient mRNA for hybridization to the glass slides, total inguinal lymph nodes RNA was pooled from three mice at each time point (2 inguinal lymph nodes per mouse). Total RNA samples were prepared using Trizol® reagent according to the manufacturers instructions. Undegraded and DNA-, protein- and phenol-free RNA preparations were verified by classic agarose gel electrophoresis stained with ethidium bromide and ultraviolet spectrophotometry, respectively.

2009-10-20 | E-MEXP-2404 | biostudies-arrayexpress

G-CSF receptor targeting in inflammatory arthritis

Project description:G-CSF is a hemopoietic growth factor that has a role in steady state granulopoiesis, as well as in mature neutrophil activation and function. We developed a neutralizing monoclonal antibody to the murine G-CSF receptor (G-CSFR), which antagonizes binding of murine G-CSF and inhibits G-CSFR signalling. Anti-G-CSFR rapidly halts the progression of established disease in collagen antibody-induced arthritis (CAbIA). Neutrophil accumulation in joints is inhibited, without rendering animals neutropenic, suggesting an effect on homing to inflammatory sites. Neutrophils in the blood and arthritic joints of anti-G-CSFR treated mice show alterations in cell adhesion receptors, while anti-G-CSFR suppresses local production of proinflammatory cytokines and chemokines known to drive tissue damage. Our aim in this study was to use differential gene expression analysis of joint and blood neutrophils to more thoroughly understand the effect of G-CSFR blockade on the inflammatory response following anti-G-CSFR therapy in CAbIA. C57BL/6 mice with collagen antibody-induced arthritis were injected intra-peritoneally at day 5 with 50 Î¼g anti-G-CSFR (n = 20 mice) or control mAb (n = 10 mice). At day 7, neutrophils (CD45+ CD11bhi Ly6G+) were sorted (BD FACSAria) from pooled digests of the knee tissues, or peripheral blood, and the RNA was extracted from 3 such experiments, giving a total of 12 samples.

2016-01-19 | E-GEOD-76966 | biostudies-arrayexpress

RNA-seq of Tfh cells from BALB/c and C57Bl/6 mice immunized with OVA-IFA or OVA-CpG

Project description:The aim of the project was the identification of the transcriptional signature of effector T cells and Tfh cells that emerge following immunization with different adjuvants. For this purpose OVA-specific TCR-transgenic cells (from DO11.10 or OT-II mice) were adoptively transferred into congenic BALB/c or C57Bl/6 mice, subsequently immunized with OVA-IFA or OVA-CpG. At day 11, the OVA-specific T effector and Tfh cells were FACS sorted from the draining lymph nodes for RNA sequencing.

2023-04-15 | E-MTAB-12086 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data