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Pathologically distinct fibroblast subsets drive inflammation and tissue damage in arthritis

ABSTRACT: Pathologically distinct fibroblast subsets drive inflammation and tissue damage in arthritis

PROVIDER: PRJNA531402 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8864040_1.fastq.gz	Fastqsanger.gz
	SRR8864040_2.fastq.gz	Fastqsanger.gz
	SRR8864050_1.fastq.gz	Fastqsanger.gz
	SRR8864050_2.fastq.gz	Fastqsanger.gz
	SRR8864060_1.fastq.gz	Fastqsanger.gz

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Pathologically distinct fibroblast subsets drive inflammation and tissue damage in arthritis

Project description:Pathologically distinct fibroblast subsets drive inflammation and tissue damage in arthritis

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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.

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Pathologically distinct fibroblast subsets drive inflammation and tissue damage in arthritis

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Functionally distinct disease-associated fibroblast subsets in rheumatoid arthritis

Project description:Functionally distinct disease-associated fibroblast subsets in rheumatoid arthritis

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Distinct fibroblast subsets drive inflammation and 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)1,2. However, it remains unclear whether fibroblast subclasses with non-overlapping functions also exist and are responsible for the wide variety of tissue-driven processes observed in IMIDs, such as inflammation and damage3-5. 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 fibroblast activation protein-? (FAP?)+ fibroblasts suppressed both inflammation and bone erosions in mouse models of resolving and persistent arthritis. Single-cell transcriptional analysis identified two distinct fibroblast subsets within the FAP?+ population: FAP?+THY1+ immune effector fibroblasts located in the synovial sub-lining, and FAP?+THY1- destructive fibroblasts restricted to the synovial lining layer. When adoptively transferred into the joint, FAP?+THY1- fibroblasts selectively mediate bone and cartilage damage with little effect on inflammation, whereas transfer of FAP?+ 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.

| S-EPMC6690841 | biostudies-literature

RNA-seq analysis of freshly isolated synovial fibroblast subsets from patients with rheumatoid arthritis

Project description:RNA-seq analysis of freshly isolated synovial fibroblast subsets from patients with rheumatoid arthritis

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Pathologically expanded peripheral B cell-helper T cells in rheumatoid arthritis

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

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miR-221/222 drive synovial fibroblast expansion and pathogenesis of TNF-mediated arthritis

Project description:MicroRNAs (miRNAs) constitute fine tuners of gene expression and are implicated in a variety of diseases spanning from inflammation to cancer. miRNA expression is deregulated in rheumatoid arthritis (RA), however, their specific role in key arthritogenic cells such as the synovial fibroblast (SF) remains elusive. We have shown in the past that the expression of the miR-221/222 cluster is upregulated in RA SFs. Here, we demonstrate that miR-221/222 activation is downstream of major inflammatory cytokines, such as TNF and IL-1β, which promote miR-221/222 expression independently. miR-221/222 expression in SFs from the huTNFtg mouse model of arthritis correlates with disease progression. Targeted transgenic overexpression of miR-221/222 in SFs of the huTNFtg mouse model led to further expansion of synovial fibroblasts and disease exacerbation. miR-221/222 overexpression altered the transcriptional profile of SFs igniting pathways involved in cell cycle progression and ECM regulation. Validated targets of miR-221/222 included p27 and p57 cell cycle inhibitors, as well as Smarca1 (a chromatin remodeling component). In contrast, complete genetic ablation of miR-221/222 in arthritic mice led to decreased proliferation of fibroblasts, reduced synovial expansion and attenuated disease. scATAC-seq data analysis revealed increased miR-221/222 gene activity in the pathogenic and activated clusters of the intermediate and lining compartment. Taken together, our results establish an SF-specific pathogenic role of the miR-221/222 cluster in arthritis and suggest that its therapeutic targeting in specific subpopulations should inform the design of novel fibroblast-targeted therapies for human disease.

2022-12-16 | GSE210887 | GEO

lncRNA and mRNA expression profiles in fibroblast-like synoviocytes from rheumatoid arthritis patients and trauma patients

Project description:Fibroblast-like synoviocytes (FLSs) are critical for synovial aggressiveness and joint destruction in rheumatoid arthritis (RA).The role and expression patterns of long noncoding RNAs (lncRNAs) in RA are largely unknown. We performed lncRNA and mRNA microarrays to identify differentially expressed lncRNAs and mRNAs in fibroblast-like synoviocytes from rheumatoid arthritis patients compared with fibroblast-like synoviocytes from trauma patients.

2018-09-07 | GSE103578 | GEO

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