ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR173/094/SRR17312494/SRR17312494.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR173/093/SRR17312493/SRR17312493.fastq.gzprimaryOK200GenomicsDepartment of Immunology, The University of Tokyohttps://www.ebi.ac.uk/ena/browser/view/PRJNA791669Mus musculusxref:PubMed:35999397xref:PubMed:35999392The 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. Overall design: scRNA-seq analysis was performed on synovial cells which were isolated from the knee joints of CIA mice (n=3) and healthy control mice (n=9). Alignment, quantitation and aggregation of the sample count matrices (CIA + control) were performed using the 10x Genomics Cell Ranger pipeline (v.3.0) according to the manufacturer’s protocol (GENEWIZ).ENAfalseTranscriptomic analysis of synovial cells derived from collagen-induced arthritis miceTranscriptomic analysis of synovial cells derived from collagen-induced arthritis mice2025-09-242022-07-08PRJNA791669GSE192504100903599939735999392