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RNA-seq analysis of synovial fibroblasts isolated from Ets1-flox/flox and Col6a1-Cre-Ets1-flox/flox mice of serum transfer-induced arthritis (STIA)

ABSTRACT: Synovial fibroblasts critically contribute to the pathogenesis of rheumatoid arthritis (RA) by acquiring either a pro-inflammatory or tissue-destructive phenotype. To explore the molecular mechanisms underlying the tissue-destructive fibroblast phenotype in arthritis, we performed bulk RNA-sequencing analysis on the synovial fibroblasts which were isolated from Col6a1-Cre-Ets1-flox/flox (Ets1ΔFib) and Ets1-flox/flox (Ets1flox) mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE201310 | GEO | 2022/07/06

REPOSITORIES: GEO

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RNA-seq analysis of synovial fibroblasts isolated from Ets1-flox/flox and Col6a1-Cre-Ets1-flox/flox mice of serum transfer-induced arthritis (STIA)

Project description:RNA-seq analysis of synovial fibroblasts isolated from Ets1-flox/flox and Col6a1-Cre-Ets1-flox/flox mice of serum transfer-induced arthritis (STIA)

| PRJNA830852 | ENA

Transcriptomic analysis of synovial cells derived from collagen-induced arthritis mice

Project description:The destruction of bone and cartilage results in a loss of joint functionality, critically impairing the quality of life in arthritis patients. Synovial fibroblasts (SFs) critically contribute to the pathogenesis of rheumatoid arthritis (RA) by acquiring either a pro-inflammatory or tissue-destructive phenotype. To explore the molecular mechanisms underlying the pathogenic fibroblast phenotype in arthritis, we performed single-cell RNA sequencing (scRNA-seq) on the synovial cells which were isolated from collagen-induced arthritis (CIA) mice.

2022-07-06 | GSE192504 | GEO

Col6a1-/- Mouse Lung

Project description:Collagen 6 (COL6) is known for its role in a spectrum of congenital muscular dystrophies, which are often accompanied by respiratory dysfunction. However, little is known regarding the function of COL6 in the lung. We confirmed the presence of COL6 throughout the basement membrane region of mouse lung tissue. We studied lung structure and organization in a previously described Col6a1-/- mouse, which do not produce detectable COL6 in the lung. The Col6a1-/- mouse displayed multiple histopathological alveolar and airway abnormalities. The airspaces of Col6a1-/- lungs appeared simplified, with larger (29%, p<0.01) and fewer (31%, p<0.001) alveoli. These airspace abnormalities included a reduction in IsolectinB4+ alveolar capillaries and Sftpc+ ATII cells. Alterations in lung function consistent with these histopathological changes were evident. Col6a1-/- mice also displayed multiple airway changes including increased branching (59%, p<0.001), increased mucosal thickness (34%, p<0.001) and increased epithelial cell density (13%, p<0.001). Comprehensive transcriptome analysis revealed loss of COL6 is associated with reductions in integrin-paxillin-PI3K signaling in vivo. In vitro, COL6 promoted steady-state phospho-paxillin levels and reduced cell density (16-28%, p<0.05) at confluence. Inhibition of PI3K, or its downstream effectors, resulted in increased cell density to a level similar to that seen on matrices lacking COL6.

2019-08-10 | GSE135667 | GEO

Col6a1-/- Mouse Lung

Project description:Col6a1-/- Mouse Lung

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Pathologically distinct fibroblast subsets drive inflammation and tissue damage in arthritis

Project description:The identification of lymphocyte subsets with non-overlapping effector functions has been pivotal to the development of targeted therapies in immune mediated inflammatory diseases (IMIDs). Yet, despite their key role in disease, it remains unclear whether fibroblast subclasses with non-overlapping functions also exist and are responsible for the wide variety of tissue driven pathologies observed in IMIDs such as inflammation and damage . Here we identify and describe the biology of distinct subsets of fibroblasts responsible for mediating either inflammation or tissue damage in arthritis. We show that deletion of FAPa+ synovial cells suppressed both inflammation and bone erosions in murine models of resolving and persistent arthritis. Single cell transcriptional analysis identified two distinct fibroblast subsets: FAPa+ THY1+ immune effector fibroblasts located in the synovial sub-lining, and FAPa+ THY1- destructive fibroblasts restricted to the synovial lining. When adoptively transferred into the joint, FAPa+ THY1- fibroblasts selectively mediate bone and cartilage damage with little effect on inflammation whereas transfer of FAPa+ THY1+ fibroblasts resulted in a more severe and persistent inflammatory arthritis, with minimal effect on bone and cartilage. Our findings describing anatomically discrete, functionally distinct fibroblast subsets with non-overlapping functions have important implications for cell based therapies aimed at modulating inflammation and tissue damage.

2019-04-09 | GSE129451 | GEO

Pathologically distinct fibroblast subsets drive inflammation and tissue damage in arthritis

2019-06-03 | GSE129087 | GEO

Sequencing of synovial tissue fibroblasts from Rheumatoid Arthritis patients that were co-cultured with inflammatory macrophages.

Project description:The role of synovial tissue fibroblasts and macrophages interactions in driving chronic inflammation and resolution of arthritis is unknown. In this project, we used bulk RNAseq to investigate the impact of different phenotypes of macrophages on activation of synovial fibroblasts.

2020-04-18 | E-MTAB-8316 | biostudies-arrayexpress

Modulation of the TNF-induced macrophage response by synovial fibroblasts

Project description:Here we explored how the human macrophage response to tumor necrosis factor (TNF) is regulated by human synovial fibroblasts, the representative stromal cell type in the synovial lining of joints that become activated during inflammatory arthritis. Genome-wide transcriptome analysis (RNAseq) showed that co-cultured synovial fibroblasts modulate the expression of approximately one third of TNF-inducible genes in macrophages, including expression of target genes in pathways important for macrophage survival and polarization towards an alternatively activated phenotype. This work furthers our understanding of the interplay between innate immune and stromal cells during an inflammatory response, one that is particularly relevant to inflammatory arthritis. Our findings also identify modulation of macrophage phenotype as a new function for synovial fibroblasts that may prove to be a contributing factor in arthritis pathogenesis.

2014-08-04 | GSE57723 | GEO

Rsk2 controls synovial fibroblast hyperplasia and the course of arthritis.

Project description:To understand differences in the pathogenesis of synovial hyperplasia during TNF-induced arthritis, we compared the global gene expression of hTNFtg and hTNFtg;Rsk2-/y primary synovial fibroblasts.

2014-12-04 | GSE52992 | GEO

Microarray analysis of freshly isolated synovial fibroblast subsets in patients with rheumatoid arthritis or osteoarthritis

Project description:Transcriptomics of distinct subpopulations of synovial fibroblasts from osteoarthritis and rheumatoid arthritis arthroplasty tissues.

2018-01-17 | GSE107105 | GEO

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