Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bulk RNA-seq on paws of collagen-induced arthritis (CIA) mouse model at different disease stages

ABSTRACT: The goal of this experiment is to profile longitudinal transcriptome changes during the development of murine arthritis in CIA mouse model. Male DBA1 mice (age between 10 to 12 weeks) were used in this study. CIA was induced by two immunizations with Type II collagen in Complete Freund’s adjuvant (CFA) at day 0, and with Type II collagen in Incomplete Freund’s adjuvant (IFA) at day 21. Bulk RNA-seq were done on right hind paws from control (non-immunized DBA1 mice) and CIA mice at different disease stages (up to 10 weeks after 1st immunization).

ORGANISM(S): Mus musculus

PROVIDER: GSE193335 | GEO | 2022/03/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

GENE EXPRESSION OF AN ANTI-INFLAMMATORY PENTAPEPTIDE ON CIA MURINE DEVELOPMENT

Project description:Monocyte Locomotion Inhibitory Factor (MLIF), an amoebic peptide, has an anti-inflammatory role, delaying the arrival of mononuclear cells to inflammatory sites, down regulating adhesin molecules and chemokines. We used microarrays to detail the global gene expression underlying anti-inflammatory effect of MILF in an inflammatory model. Collagen type II (CII) emulsified on complet Freund adjuvant, was injected on the tail of the base of DBA1J mice, 8 weeks older, and booster with CII emulsified in incomple Freund adjuvant three weeks later. MLIF was administrated intranasally weekly since one week before induction. Keywords: comparison effect Articular tissues of all mices were collected at the peak time of clinical severity (four weeks before booster), for RNA extraction and hybridization on Affymetrix microarrays. We induces CIA with chicken collagen type II, emulsified with Complet Adjuvant of Freund, and the controls were mice induced only with Complet Adjuvant of Freund with or without MLIF

2009-02-06 | E-GEOD-14721 | biostudies-arrayexpress

Identification of multiple transferrin species in spleen from mice with collagen-induced arthritis which may reflect changes in transferrin glycosylation associated with the disease activity. Role of CD38

Project description:Collagen type II-induced arthritis (CIA) is an autoimmune disease that is accompanied by a complex host systemic response, which includes inflammatory and autoimmune reactions. Since to develop CIA is required the injection of antigen in complete Freund’s adjuvant (CFA), which is a water-in-mineral-oil emulsion containing killed Mycobacteria, systemic response proteins related with inflammation can confound the detection or diagnosis of arthritis. CIA in CD38 deficient mice (CD38 KO) is milder than that in C57BL/6 (B6 WT) mice. Protein extracts from spleen were subjected to 2D-DiGE and MS-MALDI-TOF/TOF analysis to identify proteins that were differentially expressed in CD38 KO and B6 WT mice with arthritis, with inflammation, or non-immunized. Differential protein expression was validated by ELISA, or Western-blotting.

2015-12-10 | PXD002644 | Pride

2015-12-10 | PXD002643 | Pride

2015-12-11 | PXD003183 | Pride

Distinct Serum Proteome Profiles Associated with Collagen induced Arthritis, and Complete Freund’s Adjuvant-induced Inflammation in CD38-/- mice: the Discriminative Power of Protein Species or Proteoforms. Protein identification by Peptide Mass Fingerprinting (PMF)

Project description:Collagen-type-II-induced arthritis (CIA) is an autoimmune disease, which involves a complex host systemic response including inflammatory and autoimmune reactions. CIA in C57BL/6 mice resembles human rheumatoid arthritis (RA) in terms of its disease course, histological findings, and in its response to commonly used anti-arthritic drugs. In this study, the goal has been to identify proteins from serum that change in their abundance in CD38-KO versus WT mice which may reflect their distinct response to an antigen-challenge that induces the development of an autoimmune disease. CIA is milder in CD38-/- than in Wild-type (WT) mice. We analyzed the sera from CD38-/- versus WT mice either with arthritis (CIA+), with no arthritis (CIA-), or with inflammation (Complete Freund’s adjuvant (CFA)-treated mice). To decrease the dynamic concentration range of serum a combinatorial ligand library composed of hexapeptides was used (called ProteoMiner). ProteoMiner-equalized serum samples were then subjected to 2D-DiGE and MS-MALDI-TOF/TOF analyses to identify proteins that changed in their relative abundances. Multivariate analyses revealed that a multi-protein signature (n = 28) was able to discriminate CIA+ from CIA- mice, and WT from CD38-/- mice within each condition. Likewise, a distinct multi-protein signature (n = 16) was identified which differentiated CIA+ CD38-/- mice from CIA+ WT mice, and lastly, a third multi-protein signature (n = 18) indicated that CD38-/- and WT mice could be segregated in response to CFA treatment This approach allows the identification of multiple protein species, or proteoforms of a given protein in a single analysis, and therefore, to focus the interest in fully characterize just the protein species that differ in abundance.

2015-07-17 | PXD001799 | Pride

Distinct Serum Proteome Profiles Associated with Collageninduced Arthritis, and Complete Freund’s Adjuvant-induced Inflammation in CD38-/- mice: the Discriminative Power of Protein Species or Proteoforms

2015-07-17 | PXD001788 | Pride

Distinct Serum Proteome Profiles Associated with Collagen-induced Arthritis, and Complete Freund’s Adjuvant-induced Inflammation in CD38-/- mice: the Discriminative Power of Protein Species or Proteoforms. Spot 269_Spot 500

Project description:Collagen-type-II-induced arthritis (CIA) is an autoimmune disease, which involves a complex host systemic response including inflammatory and autoimmune reactions. CIA in C57BL/6 mice resembles human rheumatoid arthritis (RA) in terms of its disease course, histological findings, and in its response to commonly used anti-arthritic drugs. In this study, the goal has been to identify proteins from serum that change in their abundance in CD38-KO versus WT mice which may reflect their distinct response to an antigen-challenge that induces the development of an autoimmune disease.CIA is milder in CD38-/- than in Wild-type (WT) mice. We analyzed the sera from CD38-/- versus WT mice either with arthritis (CIA+), with no arthritis (CIA-), or with inflammation (Complete Freund’s adjuvant (CFA)-treated mice). To decrease the dynamic concentration range of serum a combinatorial ligand library composed of hexapeptides was used (called ProteoMiner). ProteoMiner-equalized serum samples were then subjected to 2D-DiGE and MS-MALDI-TOF/TOF analyses to identify proteins that changed in their relative abundances. Multivariate analyses revealed that a multi-protein signature (n = 28) was able to discriminate CIA+ from CIA- mice, and WT from CD38-/- mice within each condition. Likewise, a distinct multi-protein signature (n = 16) was identified which differentiated CIA+CD38-/- mice from CIA+ WT mice, and lastly, a third multi-protein signature (n = 18) indicated that CD38-/- and WT mice could be segregated in response to CFA treatment This approach allows the identification of multiple protein species, or proteoforms of a given protein in a single analysis, and therefore, to focus the interest in fully characterize just the protein species that differ in abundance.

2015-07-17 | PXD002071 | Pride

GENE EXPRESSION OF AN ANTI-INFLAMMATORY PENTAPEPTIDE ON CIA MURINE DEVELOPMENT

2009-02-07 | GSE14721 | GEO

Mouse CIA Cytokine Array

Project description:The molecular basis to autoimmune arthritis is unclear. Collagen Induced Arthritis (CIA) in mice, is a model that has many features that resemble Rheumatoid Arthritis (RA), although it does not perfectly duplicate RA. The study of CIA has provided insight into relevant pathogenesis and has aided in the identification of potential therapeutic targets. In this study we used Mouse Cytokine Expression Arrays to examine gene expression levels in joints at early, peak and decline stages during disease in DBA/1 mice. The aim of the study was to identify candidate molecules that may be involved in the development and progression of collagen-induced arthritis (CIA). Keywords: Disease State Analysis

2007-09-18 | GSE8915 | GEO

Collagen induced arthritis in dba/1j mice associates with oxylipin changes in plasma

Project description:Oxylipins play important roles in various biological processes and are considered as mediators of inflammation for a wide range of diseases such as rheumatoid arthritis (RA). The purpose of this research was to study differences in oxylipin levels between a widely used collagen-induced arthritis (CIA) mice model and healthy control (Ctrl) mice. DBA/1J male mice (age: 6-7 weeks) were selected and randomly divided into two groups, viz. a CIA- and a Ctrl group. The CIA mice were injected intraperitoneal (i.p.) with the joint cartilage component collagen type II (CII) and an adjuvant injection of lipopolysaccharide (LPS). Oxylipin metabolites were extracted from plasma for each individual sample using solid phase extraction (SPE) and were detected with high performance liquid chromatography/tandem mass spectrometry (HPLC-ESI-MS/MS), using dynamic multiple reaction monitoring (dMRM). Both univariate and multivariate statistical analysis was applied. The results in univariate student's t-test revealed 10 significantly up- or down-regulated oxylipins in CIA mice, which were supplemented by another 6 additional oxylipins, contributing to group clustering upon multivariate analysis. The dysregulation of these oxylipins revealed the presence of ROS-generated oxylipins and an increase of inflammation in CIA mice. The results also suggested that the Collagen-induced arthritis might associate with dysregulation of apoptosis, possibly inhibited by activated NF- κ B because of insufficient PPAR-γ ligands.

2015-11-04 | MTBLS243 | MetaboLights

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