Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell RNA sequencing of knee joint synovium from mice with collagen- and antibody-induced arthritis (C&AIA)

ABSTRACT: Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation, immune cell infiltration, and progressive joint destruction. Commonly used mouse models each carry practical constraints: collagen-induced arthritis (CIA) is largely restricted to the DBA/1 strain, whereas collagen antibody-induced arthritis (CAIA) is limited by antibody cost. To combine strain flexibility with a robust and reproducible effector phase, we established collagen- and antibody-induced arthritis (C&AIA) on the C57BL/6 background. To characterize the synovial cellular landscape of this model, we performed droplet-based single-cell RNA sequencing on synovial tissue dissected from inflamed knee joints of arthritic C&AIA mice. This dataset resolves the immune and stromal compartments of the C&AIA synovium and enables cross-species comparison with human RA synovial single-cell data.

ORGANISM(S): Mus musculus

PROVIDER: GSE341410 | GEO | 2026/07/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

gene expression profiles in ankles from CAIA mice model

Project description:To identify a candidate epigenetic regulator in RA pathogenesis, gene expression microarray analysis was conducted using mRNA obtained from whole ankle tissue in collagen antibody-induced arthritis (CAIA) mice and two control mice (CtrlP and CtrlL)

2022-05-16 | GSE167190 | GEO

Arthritis protection conferred by a subset of antibodies to citrullinated proteins in rheumatoid arthritis - human synovium fluids samples

Project description:Anti-citrullinated protein antibodies (ACPAs) are one of the hallmarks in rheumatoid arthritis (RA), but the in vivo function remained unclear. To investigate the effects of ACPAs, we expressed monoclonal ACPAs derived from RA patients, and analyzed the functions in mouse models, as well as the reactivity to tissue and peptides/proteins. All ACPAs showed no arthritogenicity and could not induce pain-like behavior in mice whereas one of them (E4) profoundly protected against antibody-induced arthritis. E4 showed a tissue binding pattern restricted to skin epithelial cells, to macrophages and dendritic cells in lymphoid tissue and to cartilage from mouse and human arthritic joints. Proteomic analysis showed that E4 had a distinct binding pattern to macrophage and RA synovial fluid proteins (e.g. alpha-enolase). The protective effect was epitope specific but also dependent on Fc-FCGR2B interaction on macrophages following the immune complex formation, resulting an increased IL-10 production and osteoclastogenesis reduction. The findings suggest that certain ACPAs could be protective in arthritis with therapeutic potentials.

2023-01-09 | PXD035180 | Pride

Bone-protective effects of neutralizing angiopoietin-like protein 4 monoclonal antibody in rheumatoid arthritis

Project description:Despite recent advances, rheumatoid arthritis (RA) patients remain refractory to therapy. Dysregulated overproduction of angiopoietin-like protein 4 (ANGPTL4) is thought to contribute to the disease development. ANGPTL4 was initially identified as a regulator of lipid metabolism, which is hydrolyzed to N-terminal and C-terminal (cANGPTL4) fragments in vivo. cANGPTL4 is involved in several non-lipid-related processes, including angiogenesis and inflammation. This study revealed that the level of ANGPTL4 was markedly elevated in the sera and synovial tissues from patients with RA versus controls. The administration of a neutralizing antibody against cANGPTL4 (anti-cANGPTL4 Ab) resulted in the inhibition of inflammatory processes and bone loss in animal models of collagen-induced arthritis and adjuvant-induced arthritis (AIA). Transcriptomic and proteomic profiling of synovial tissues from an AIA model indicated that the anti-cANGPTL4 Ab inhibited fibroblast-like synoviocyte (FLS) immigration and inflammatory-induced osteoclastogenesis. Mechanistically, the anti-cANGPTL4 Ab has been shown to inhibit TNF-α-induced inflammatory cascades in RA-FLS through the sirtuin 1/nuclear factor-κB signaling pathway. Moreover, the anti-cANGPTL4 Ab was found to block FLS invasion- and immigration-induced osteoclast activation. Collectively, these findings identify ANGPTL4 as a prospective biomarker for the diagnosis of RA, and targeting cANGPTL4 should represent a potential therapeutic strategy.

2024-10-24 | GSE276556 | GEO

Hyperactive lateral habenula mediates the comorbidity between rheumatoid arthritis and depression-like behaviors

Project description:Objective: The aim of this study was to identify the neural and molecular mechanisms underlying the comorbidity of rheumatoid arthritis (RA) and depression. Methods: A cohort of 200 RA patients were recruited to quantitatively assess the association between depressive symptoms and RA disease activity, as well as quality of life. The collagen antibody-induced arthritis (CAIA) mouse model of RA was used to screen for brain regions that showed changes in c-FOS expression, an indicator of alteration in brain activity, accompanying the appearance of depression-like behaviors. RNA sequencing, immunostaining, AAV-mediated expression, micro-CT, plasma cytokines/chemokines measurements and histological analyses were applied to evaluate the contribution of the identified brain region in the disease progression of RA and depression-like symptoms. Results: In this study, we showed that in RA patients, the depression scores were significantly correlated with the severity and quality of life of the patients. The CAIA mice developed RA symptoms, together with depression-like behaviors accompanied by hyperactivity and alterations in gene expression reflecting cerebrovascular disruption in the lateral habenula (LHb), a brain region processing negative valence. Importantly, inhibition of the LHb outputs not only alleviated depression-like behaviors, but also resulted in rapid remission of RA symptoms and reduction in sympathetic nerve fibers in the synovial joints of the CAIA mice.Conclusion: Our study highlights a critical but previously overlooked contribution of hyperactive LHb to the comorbidity between RA and depression, suggesting that targeting LHb in conjunction with RA treatments may be a promising strategy for RA patients comorbid with depression.

2025-08-30 | GSE241929 | GEO

Rheumatoid Synovial Subsets of CD3+ T cells defined by PD-1+ and PD-1- Cells Drive Fibroblasts into Distinct Endotypes

Project description:Introduction: The joint destructive process in rheumatoid arthritis (RA) is highly individual and dominated by complex cellular interactions. In damping the immune activation, the PD-1 pathway is central and highly upregulated in the arthritic joint. Here, we examine how T cells with or without PD-1 influence the function of arthritic mesenchymal cells Methods: We investigated samples from RA synovial fluid and characterized PD-1+ and PD-1- T cells by flow cytometry, ELISA and RNA sequencing (RNA seq). We performed co-culture experiments to investigate the interaction between PD-1+/- cells, osteoclasts, osteoblasts and fibroblasts. We used flow cytometry, ELISA and RNA seq to characterize the RA and HC fibroblasts after co-culture with PD-1+ and PD-1- T cells. Results: We found PD-1+ T cells to express other checkpoint receptors and to have a diminished cytokine production upon CD3/CD28 stimulation. The PD-1+ and PD-1- T cells from the RA synovial fluid clustered differently after RNA seq, and the gene signature of the PD-1+ T shared traits with peripheral T helper cells. Fibroblasts co-cultured with PD-1+ T cells expressed genes associated with collagen synthesis, TGFbeta production and immune regulation. In contrast, the signature in fibroblasts co-cultured with PD-1- cells was associated with immune activation. Conclusion: We demonstrate RA synovial fluid CD3+ T cell subsets can drive healthy fibroblasts into distinct pathological endotypes. When evaluating all PD-1+ T cells, these support fibroblast subsets related to the production of collagen and immune regulation.

2025-11-27 | E-MTAB-15969 | biostudies-arrayexpress

The Anti-Arthritis Effect of Olive-Derived Maslinic Acid in Mice is Due to its Promotion of Tissue Formation and its Anti-Inflammatory Effects.

Project description:SCOPE: A previous study demonstrated that intake of olive pomace extract containing maslinic acid (MA), a triterpene, effectively prevents and alleviates arthritis in animals and humans. Here, the molecular mechanisms involved in the anti-arthritis effect of MA have been elucidated by determining gene expression changes induced by olive-derived MA intake in collagen antibody-induced arthritis (CAIA) mice. METHODS AND RESULTS: Mice are divided into the untreated (CT), CAIA (CA), and CAIA administered MA (CA + MA) groups. The CA + MA mice are fed MA at a daily dose of 200 mg kg-1 of body weight from day 1. CAIA is then induced on day 8 and evaluated on day 12. Arthritis symptoms are alleviated, and the gene expression of inflammatory cytokines is reduced in the CA + MA group compared with the CA group. A DNA microarray analysis of synovial membranes reveals that MA alters the expression levels of genes related to inflammation, including glucocorticoid responses, immune responses, and the extracellular matrix. CONCLUSIONS: The preventive effect of MA on arthritis is attributable to the promotion of tissue formation as well as suppression of inflammation in the synovium via inactivation of Toll-like receptor signaling and downregulation of leukotrienes through the glucocorticoid receptor.

2019-03-22 | GSE111096 | GEO

Bone-protective effects of neutralizing angiopoietin-like protein 4 monoclonal antibody in rheumatoid arthritis

Project description:Despite recent advances, rheumatoid arthritis (RA) patients remain refractory to therapy. Dysregulated overproduction of angiopoietin-like 4 protein (ANGPTL4) is thought to be contributed to the disease development. Therefore, interference with ANGPTL4 biological function may constitute a new therapeutic strategy for this disease. ANGPTL4 was initially identified as a regulator of lipid metabolism, which is hydrolyzed to N-terminal (nANGPTL4) and C-terminal (cANGPTL4) fragments in vivo. cANGPTL4 is involved in several non-lipid-related processes, including angiogenesis and inflammation. In this study, we analyzed the mRNA expression of ANGPTL4 in synovial tissue of RA in comparison to healthy individuals of the Gene Expression Omnibus (GEO) database. The results indicated that the mRNA expression of ANGPTL4 is increased in RA synovial tissues. The level of ANGPTL4 was found to be overexpressed in the sera and synovial tissues from patients with RA versus controls. A neutralizing antibody against cANGPTL4 (anti-cANGPTL4 Ab) was employed to treat arthritis animal models, including collagen-induced arthritis (CIA) and adjuvant-induced arthritis (AIA), respectively. The results demonstrated that the anti-cANGPTL4 Ab inhibited inflammation and bone loss in two models. Transcriptomic and proteomic profiling of synovial tissues from AIA model indicated that the anti-cANGPTL4 Ab inhibited fibroblast-like synoviocyte (FLS) immigration and inflammatory-induced osteoclastogenesis. These data collectively identify ANGPTL4 as a potential biomarker for the diagnosis of RA, and targeting cANGPTL4 may represent a novel therapeutic strategy.

2024-09-05 | PXD055569 |

Transcriptome analysis of synovial osteoprogenitor populations in mice with antigen-induced arthritis and non-immunized mice

Project description:The aim of this experiment was to analyze differences in gene expression between potential osteoprogenitor populations in synovial compartment of non-immunized mice and mice with antigen-induced arthritis (AIA). We analyzed transcriptome of TER119–CD31–CD45–CD51+CD200+CD105– cells from nonimmunized mice, TER119–CD31–CD45–CD51+CD200+CD105– cells from mice with arthritis, and TER119–CD31–CD45–CD51+CD200–CD105+ from mice with arthritis. Comparison between nonimmunized and arthritic mice served to determine changes in TER119–CD31–CD45–CD51+CD200+CD105–population induced by arthritis. Comparison of TER119–CD31–CD45–CD51+CD200+CD105– and TER119–CD31–CD45–CD51+CD200–CD105+ from mice with arthritis aimed to define transcriptomic differences between those two populations.

2020-05-05 | GSE148130 | GEO

Arthritis protection conferred by a subset of antibodies to citrullinated proteins in rheumatoid arthritis - macrophage samples

2023-01-09 | PXD035177 | Pride

miRNA Expression data from synovium in mouse serum transfer arthritis model (STA) model

Project description:To find regulated miRNAs during peak inflammation of rheumatoid arthritis (RA), we have collected synovium from mouse STA model at day 0 (Non Arthritic) and day 10 (Peak Inflammation). For miRNA profiling, we used high-throughput BioMark Real-Time PCR system (Fluidigm, South San Francisco, CA)

2016-09-28 | GSE71600 | GEO

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