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

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

PROVIDER: PRJNA791669 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17312493.fastq.gz	Fastqsanger.gz
	SRR17312494.fastq.gz	Fastqsanger.gz

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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.

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The differentially expressed circular RNA (circRNA) in Collagen-induced arthritis rats compared with normal rats.

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Project description:We observed resolution of inflammatory response in collagen-induced arthritis (CIA) mice. To identify molecular signatures defining resolution of the CIA, we applied microarray analysis for synovial tissues in the CIA mice in 6 (induction), 9 (peak) and 15 weeks (resolution) after immunization. To identify genes related to CIA resolution, we performed the following comparisons of gene expression profiles: peak versus induction phase and resolution versus peak phase. We identified that three genes, Itgb1, Ywhaz and Rps3, are the key regulators for the resolution by measuring degree, betweenness and closeness centrality in reconstructed network based on protein-protein interaction data. To confirm this result, we compared the gene and protein expression level of the three regulators between the two phases of inflammation. Furthermore, we showed that the gene and protein expression level of the three regulators are up-regulated in regulatory T cells and type 2 macrophages than other subtypes of CD4+ T cells and macrophages, and also we examined that recombinant peritoneal macrophages of the three regulators can modulate the expression of pro-inflammatory and anti-inflammatory cytokines. Thus, our findings suggest that those regulators can be employed as therapeutic uses for resolving inflammation

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