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Multi-organ single cell analysis of a mouse model of collagen-induced arthritis [subseries1]

ABSTRACT: Multi-organ single cell analysis of a mouse model of collagen-induced arthritis [subseries1]

PROVIDER: PRJNA851728 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19782222.fastq.gz	Fastqsanger.gz
	SRR19782223.fastq.gz	Fastqsanger.gz
	SRR19782224.fastq.gz	Fastqsanger.gz
	SRR19782225.fastq.gz	Fastqsanger.gz
	SRR19782226.fastq.gz	Fastqsanger.gz

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Multi-organ single cell analysis of a mouse model of collagen-induced arthritis

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Multi-organ single cell analysis of a mouse model of collagen-induced arthritis [subseries2]

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Multi-organ single cell analysis of a mouse model of collagen-induced arthritis [subseries1]

Project description:Prioratization of disease associated mechanisms in immune-mediated inflammatory diseases (IMIDs) is complicated by altered interactions across multiple organs and cell types. We have adressed these challenges by analyzing a multi-organ multicellular disease model (MO-MCDM) of a mouse IMID model, namely collagen-induced arthritis (CIA). For all the five organs (joint, lung, muscle, skin, and spleen) we found highly complex and heterogenous expression changes due to disease, although, macroscopic and microscopic signs of inflammation could only be seen in joints. Based on the MO-MCDM, predicted molecular interactions within and between organs could be identified. The model supported that inflammation was switched on or off in different organs, by an altered balande between pro- and anti-inflammatory upstream regulators and downstream pathways. This on/off switch was validated in human IMIDs, by analyses of publically available data from 32 different samples of 10 different IMIDs. Additionally, it showed consistency with a general characteristic of both CIA and human IMIDs, namely variable organ involvement in disease.

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Multi-organ single cell analysis of a mouse model of collagen-induced arthritis [subseries2]

Project description:Prioratization of disease associated mechanisms in immune-mediated inflammatory diseases (IMIDs) is complicated by altered interactions across multiple organs and cell types. We have adressed these challenges by analyzing a multi-organ multicellular disease model (MO-MCDM) of a mouse IMID model, namely collagen-induced arthritis (CIA). In this pilot study, we sequenced at least one healthy and one CIA sample from each of the ten organs, joint, lung, muscle, skin, spleen, blood, draining lymph nodes, thymus, liver, and kidney. Sequencing data from liver and kidney never reached our defined quality cut-off, and were thus excluded from further comparisions. Of the remaining organs, we found that joint, lung, muscle, skin, and spleen had the highest number of DEGs between CIA and healthy mice. We thus reason that these five organs shoult be most relevant to study disease associated changes on a systemic level, and prioritized those for further analyses.

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HIF2α-regulated genes in small intestine epithelial cells from collagen induced arthritis model

Project description:HIF2α works as an important transcription factor to induce target genes mediating cell proliferation, meabolism and inflammation. To gain new insights into HIF2α modulated genes, we used high-throughput sequencing to analyze potential HIF2a regulated genes in small intestine cells from collagen induced arthritis model mice.

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Project description:The aim of the project is to analyze the plasma proteomic profile of an animal model of arthritis (Collagen Induced Arthritis; CIA) in response to different treatments. For this, plasma samples from mice under five different treatments were analyzed (N=6 per group): Vehicle, CIA, CIA + Δ9-THCA-A (20 mg / kg), CIA + Δ9-THCA-A (20 mg / kg) + T0070907 (5 mg / kg) and CIA + Δ9-THCA-A (20 mg / kg) + SR141716A (5 mg / kg).

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