RNA sequencing in arthritic joints of wild type and Sema3B deficient mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA766408 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16074271.fastq.gz | Fastqsanger.gz | |||
| SRR16074272.fastq.gz | Fastqsanger.gz | |||
| SRR16074273.fastq.gz | Fastqsanger.gz | |||
| SRR16074274.fastq.gz | Fastqsanger.gz | |||
| SRR16074275.fastq.gz | Fastqsanger.gz |
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Project description:We found that the severity of the K/BxN serum-transfer arthritis model is higher in Sema3B deficient (Sema3b-/-) mice. Here we analyzed by RNAseq the tranciptional differences in the joints of these mice group. We used four groups: 1) WT control (non-arthritic); 2) Sema3b-/- control; 3) WT arthritis day 9; 4) Sema3b-/- artritis day 9.
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Project description:GOAL: Identification of genes and/or pathways involved in the pathogenesis of animal models of Rheumatoid Arthritis (RA). Total RNA samples were extracted from synovial fibroblast ex vivo cultures or whole joints (J), isolated from arthritic mice (197, DARE) and their corresponding normal (F1, wt) littermates. Fluorescent-labeled cRNA probes were utilized to hybridize (in duplicates for 197, indicated by "new") the Affymetrix Mu11K oligonucleotide DNA chipset (A+B). In detail the samples are:<br> <table> <tr> <td> <u>Animal model</u> </td> <td> <u>Sample source</u> </td> <td> <u>Sample name</u> </td> </tr> <tr> <td> Tg197 </td> <td> Tg197 ex-vivo cultured synoviocyte populations </td> <td> 197 </td> </tr> <tr> <td> Tg197 </td> <td> Tg197 ex-vivo cultured synoviocyte populations </td> <td> 197new </td> </tr> <tr> <td> Tg197 </td> <td> wt ex-vivo cultured synoviocyte populations </td> <td> F1 </td> </tr> <tr> <td> Tg197 </td> <td> wt ex-vivo cultured synoviocyte populations </td> <td> F1new </td> </tr> <tr> </tr> <tr> <td> Tg197 </td> <td> Tg197 whole joints </td> <td> 197J </td> </tr> <tr> <td> Tg197 </td> <td> Tg197 whole joints </td> <td> 197Jnew </td> </tr> <tr> <td> Tg197 </td> <td> wt whole joints </td> <td> F1J </td> </tr> <tr> <td> Tg197 </td> <td> wt whole joints </td> <td> F1Jnew </td> </tr> <tr> </tr> <tr> <td> DARE </td> <td> DARE ex-vivo cultured synoviocyte populations </td> <td> DARE </td> </tr> <tr> <td> DARE </td> <td> wt ex-vivo cultured synoviocyte populations </td> <td> wt </td> </tr> <tr> <td> DARE </td> <td> DARE whole joints </td> <td> DAREJ </td> </tr> <tr> <td> DARE </td> <td> wt whole joints </td> <td> wtJ </td> </tr> </table> <br> Submitted files carry the extension A or B, corresponding to the subArrays of chipset Mu11K. Arthritic samples were always compared with the corresponding wt sample and not to a common reference chip.
2005-06-30 | E-MEXP-255 | biostudies-arrayexpress
Project description:Rheumatoid arthritis is an autoimmune disease in which joint inflammation lead to progressive cartilage and bone destruction. Matrix metalloproteinases (MMP) implicated in homeostasis of extracellular matrix (ECM) play a central role in cartilage degradation. The aim of this study was to investigate the role of MMP-8 (collagenase-2) suppression in the K/BxN serum-transfer arthritis model. Three male mice of each following groups: MMP-8 wild type and arthritic mice, MMP-8 wild type without arthritis (wild type control), MMP-8 KO and arthritic mice and MMP-8 KO without arthritis (KO control) were selected for RNA extraction, from ankle joints, and hybridation on Affymetrix microarrays. Male mice were used because they showed a trend to higher arthritis severity compared to female mice. In arthritic mice, ankle joints were taken 7 days after arthritis induction.
2010-07-17 | E-GEOD-22971 | biostudies-arrayexpress
Project description:RNAseq analysis of wildtype and Slc7a5 knockout CD4+ T cells from the knee joints of arthritic mice
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Project description:We report differences in gene expression between wildtype and Slc7a5 knockout CD4+ T cells obtained from mouse knee joints with antigen induced arthritis
2022-12-21 | GSE168750 | GEO
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
Project description:Rheumatoid arthritis (RA) is a heterogeneous disease with clinical and biological polymorphisms. However, little is known about baseline molecular variations among individual RA patients. The purpose of this study was to address this issue using F2 intercross mice generated from arthritis-prone BALB/c and arthritis-resistant DBA/1 mice deficient for interleukin 1 receptor antagonist (Il1rn). Two distinct subpopulations of arthritic mice were identified in the 38 mice studied. One subgroup of diseased mice was characterized by myeloid cell dominant inflammation, whereas the other was mainly associated with increased anti-apoptotic activities of inflammatory cells. Keywords: disease state analysis
2008-07-31 | GSE8690 | GEO
Project description:Background: Unbiased studies using different genome-wide methods have identified several promising novel biomarkers for diagnosis and treatment response in Rheumatoid Arthritis (RA). However, clinical translation has proven difficult. Here, we hypothesized that one reason could be that inflammatory responses in peripheral blood are different from those in the arthritic joint. Methods: We performed meta-analysis of gene expression microarray data from synovium, whole blood cells (WBC), peripheral blood mononuclear cells (PBMC), and CD4+ T cells from patients with RA and healthy control in order to identify overlapping pathways, predicted upstream regulators and potential biomarkers. We also analyzed single cell RNA-sequencing (scRNA-seq) data from peripheral blood and whole joints from a mouse model of antigen-induced arthritis. Results: Analyses of two profiling data sets from synovium from RA patients and healthy controls all showed significant activation of pathways of known pathogenic relevance, such as Th1 pathway, role of NFAT in regulation of the immune response, dendritic cell maturation, iCOS-iCOSL signaling in T helper cells, Fc? receptor-mediated phagocytosis, interferon signaling, Cdc42 signaling, and cytotoxic T lymphocyte-mediated apoptosis. The most activated upstream regulators included TNF, an important drug target, as well as IFN-gamma and CD40LG, all of which are known to play important pathogenic roles in RA. The differentially expressed genes from synovium included several potential biomarkers, such as CCL5, CCL13, CCL18, CX3CL1, CXCL6, CXCL9, CXCL10, CXCL13, IL15, IL32, IL1RN, SPP1, and TNFSF11. By contrast, microarray studies of WBC, PBMC and CD4 + T cells showed variable pathways and limited pathway overlap with synovium. Similarly, scRNA-seq data from a mouse model of arthritis did not support that inflammatory responses in peripheral blood reflect those in the arthritic joints. These data showed pathway overlap between mouse joint cells and synovium from patients with RA, but not with cells in peripheral blood. Conclusions: Our findings indicate a dichotomy between gene expression changes, pathways, upstream regulators and biomarkers in synovium and cell types in peripheral blood, which complicates identification of biomarkers in blood.
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Project description:Troxerutin (TXR), a potent antioxidant compound shows anti-inflammatory activity and possesses hepatoprotective effect. In this study, we aimed to exploit its anti-arthritic properties using adjuvant induced arthritic model. Using relative quantitative proteomics approach, we also tried to understand the mode of action of TXR at mechanistic details and its possible usage in the treatment of arthritis. Results provide a set of candidate biomarkers for responses to TXR in the arthritis and suggest new modalities of anti-arthritic activities. A number proteins were identified from the joint homogenates of the experimental rats using isobaric tag for relative and quantitative proteomics (iTRAQ) method. The detailed study and validation of these proteins involved may be useful in finding out newer treatment modalities.
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