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Circulating proinflammatory cytokines alter transcriptional activity within fibrotic tissue of Dupuytren’s disease patients

ABSTRACT: Circulating proinflammatory cytokines alter transcriptional activity within fibrotic tissue of Dupuytren’s disease patients

PROVIDER: PRJNA716676 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14053649_1.fastq.gz	Fastqsanger.gz
	SRR14053649_2.fastq.gz	Fastqsanger.gz
	SRR14053650_1.fastq.gz	Fastqsanger.gz
	SRR14053650_2.fastq.gz	Fastqsanger.gz
	SRR14053651.fastq.gz	Fastqsanger.gz

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Circulating proinflammatory cytokines alter transcriptional activity within fibrotic tissue of Dupuytren’s disease patients

Project description:In this project, we have utilized blood and tissue samples from patients with Dupuytren’s disease (DD), a common fibroproliferative disorder of the hand, to identify increased circulating proinflammatory cytokines and assess alterations in the tissue using RNAseq and FTIR analysis. Our results indicate that specific cytokines in circulation play a direct role in local disease progression and may be useful for prospective identification of patients at risk for disease progression or recurrence as well as the development of novel therapeutic strategies. Furthermore, these results help to mechanistically link the well understood association of DD with chronic low-grade inflammatory states.

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Project description:Exposure to proinflammatory cytokines is believed to contribute to pancreatic β-cells during diabetes development. While some cytokine-mediated changes in islet gene expression are known, the heterogeneity of the response is not well-understood. Following 6 hour treatment with interleukin-1 beta (IL-1β) and interferon-gamma (IFN-γ) alone or together, mouse islets were subjected to single-cell RNA-sequencing (scRNA-seq). Inducible nitric oxide synthase (iNOS) mRNA (Nos2), antiviral genes, and immune-associated genes were induced in a subset of β-cells in response to both cytokines, while IL-1β alone activated only antiviral genes. Subsets of α- and δ-cells expressed Nos2 and exhibited similar gene expression changes as β-cells, including induction of antiviral genes and repression of identity genes. Finally, cytokine-responsiveness was inversely correlated with expression of genes encoding heat shock proteins. Our findings show that all endocrine cell types respond to cytokines, IL-1β induces the expression of protective genes in β-cells, and cellular stress gene expression is associated with an inhibition in cytokine signaling.

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