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Transcriptomic Landscape of Fibroblasts Under IL-1β Stimulation [ATAC-seq]

ABSTRACT: Transcriptomic Landscape of Fibroblasts Under IL-1β Stimulation [ATAC-seq]

PROVIDER: PRJNA1148625 | ENA |

REPOSITORIES: ENA

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Transcriptomic Landscape of Fibroblasts Under IL-1β Stimulation [ATAC-seq]

Project description:In this study, we investigated the chromatin accessibility changes in human dermal fibroblasts in response to IL-1尾 stimulation, a key pro-inflammatory cytokine. Using ATAC-seq, we compared the open chromatin landscapes between control fibroblasts and those treated with IL-1尾. The data provide insights into the regulatory elements activated during fibroblast differentiation and their potential role in sustaining inflammation within the skin. These findings contribute to our understanding of fibroblast-mediated inflammation in autoimmune diseases like SLE and offer a resource for identifying novel therapeutic targets.

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Project description:To gain a better understanding of the role of Interleukin-1β (IL-1β) in lung CD140a+ mesenchymal cells (fibroblasts) modulation, we performed RNA-seq to compare the transcriptomes of IL-1β-treated and control lung CD140a+ mesenchymal cells (fibroblasts).

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Effect of IL-1β on gene expression of human dermal fibroblasts

Project description:Fibroblasts display significant heterogeneity and exhibit distinct gene expression profiles under different cytokine stimulations. We utilized RNA-seq to analyze the expression profile differences between control and IL-1β stimulated fibroblasts（ n=3）. Our analysis revealed 1756 differentially expressed genes between WT and Smyd1-KO hearts [adjusted P-value <0.05, |log2(fold change)| > 0.5]. Among these, 755 genes were upregulated, and 843 genes were downregulated in IL-1β stimulated human dermal fibroblasts. Notably, IL-1β stimulation can induce fibroblast differentiation into pro-inflammatory fibroblasts, characterized by the expression of neutrophil-related chemokines (CXCL1, CXCL2, CXCL3), ferroptosis-related genes (PTGS2, TNFAIP6), and pro-inflammatory cytokines (IL6). Our findings lay the groundwork for understanding the IL-1β-induced fibroblast expression of specific gene profiles.

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Transcriptome analysis in primary fibroblasts from HOIL-1-deficient patients upon TNF-α or IL-1β stimulation

Project description:HOIL-1 deficient disease is a new early onset fatal autosomal recessive human disorder charaterized by chronic auto-inflammation, recurrent invasive bacterial infections and progressive muscular amylopectinosis. We studied the effect of TNF-α and IL-1β on transcriptional changes of primary fibroblasts from HOIL-1-, MYD88- and NEMO-deficient patients. Primary fibroblasts were obtained from HOIL-1, MYD88- and NEMO-deficient patients and healthy donors and stimulated with TNF-α or IL-1β for 2 and 6 hours. RNA were extracted and globin reduced. Labeled cRNA were hybridized to Illumina Human HT-12 Beadchips.

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Neutrophil modulation by IL-1β-induced fibroblasts

Project description:Neutrophil modulation by IL-1β-induced fibroblasts

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Neutrophil modulation by IL-1β-induced fibroblasts

Project description:Neutrophils are key contributors to the pathogenesis of SLE. Using single-cell sequencing data from SLE skin lesions, we identified a subcluster of CXCL1+ fibroblasts primarily induced by IL-1β. To better understand the effects of CXCL1+ fibroblasts on neutrophils, we established a conditional culture model using culture supernatants from control and IL-1β-stimulated fibroblasts. Neutrophils were collected after 21 hours of conditional culture and subjected to RNA-seq. Our findings revealed that neutrophils exhibited a distinct pro-inflammatory phenotype, expressing higher levels of pro-inflammatory cytokines such as IL1B, TNFA, IL8, and OSM.

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IL-36R stimulation of colonic mouse fibroblasts

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RNA-seq of ex vivo cultured lung CD140a+ mesenchymal cells (fibroblasts) upon stimulation by IL-1β

Project description:RNA-seq of ex vivo cultured lung CD140a+ mesenchymal cells (fibroblasts) upon stimulation by IL-1β

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The role of IRAKM in IL-1β-treated adipocytes

Project description:Toll-like receptors/Interleukin-1 receptor (IL-1R) signaling plays an important role in High-fat diet (HFD)-induced adipose tissue dysfunction contributing to obesity-associated metabolic syndromes. Here, we show an unconventional IL-1R-IRAKM (IL-1R-associated kinase M)-Slc25a1 signaling axis in adipocytes that reprograms lipogenesis to promote diet-induced obesity. Adipocyte-specific deficiency of IRAKM reduced HFD-induced body weight gain, increased whole body energy expenditure and improved insulin resistance, associated with decreased lipid accumulation and adipocyte cell sizes. IL-1β stimulation induced the translocation of IRAKM Myddosome to mitochondria to promote de novo lipogenesis in adipocytes. Mechanistically, IRAKM interacts with and phosphorylates mitochondrial citrate carrier Slc25a1 to promote IL-1β-induced mitochondrial citrate transport to cytosol and de novo lipogenesis. Moreover, IRAKM-Slc25a1 axis mediates IL-1β induced Pgc1a acetylation to regulate thermogenic gene expression in adipocytes. IRAKM kinase-inactivation also attenuated HFD-induced obesity. Taken together, our study suggests that the IL-1R-IRAKM-Slc25a1 signaling axis tightly links inflammation and adipocyte metabolism, indicating a novel therapeutic target for obesity.

2022-06-09 | PXD031934 | Pride

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