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Interepithelial inflammatory crosstalk mediated by stromal fibroblast communication through hyaluronan [dataset 1]

ABSTRACT: Interepithelial inflammatory crosstalk mediated by stromal fibroblast communication through hyaluronan [dataset 1]

PROVIDER: PRJNA666783 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12755775_1.fastq.gz	Fastqsanger.gz
	SRR12755775_2.fastq.gz	Fastqsanger.gz
	SRR12755776_1.fastq.gz	Fastqsanger.gz
	SRR12755776_2.fastq.gz	Fastqsanger.gz

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Interepithelial inflammatory crosstalk mediated by stromal fibroblast communication through hyaluronan [dataset 2]

Project description:Interepithelial inflammatory crosstalk mediated by stromal fibroblast communication through hyaluronan [dataset 2]

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Interepithelial inflammatory crosstalk mediated by stromal fibroblast communication through hyaluronan

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Interepithelial inflammatory crosstalk mediated by stromal fibroblast communication through hyaluronan [dataset 2]

Project description:Inflammation of epithelial structures frequently leads to disease at distal organs, but the mechanism responsible for this is unknown. We report evidence that digestion of hyaluronan in the extracellular matrix signals distal stromal cells to become primed for increased inflammation. By applying transgenic mouse models and single cell RNA sequencing of mouse and human tissues we demonstrate that skin injury or infection promotes an adipogenic response in distinct populations of distant submucosal fibroblasts of the colon. This response can be recapitulated without skin inflammation by expression of hyaluronidase in skin that promotes a highly amplified and frequently fatal host response to intestinal injury. Our results uncover an innate system of communication between epithelial stroma that is not initiated by immunocyte trafficking or cytokine signaling.

2020-10-19 | GSE158989 | GEO

Interepithelial inflammatory crosstalk mediated by stromal fibroblast communication through hyaluronan [dataset 1]

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Interepithelial inflammatory crosstalk mediated by stromal fibroblast communication through hyaluronan

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-10-19 | GSE159509 | GEO

Celastrol targets LRP1 to inhibit fibroblast-macrophage crosstalk and ameliorates psoriasis progression

Project description:In the present study, we analyzed single-cell multi-omics data from psoriasis patients and healthy individuals and found that more fibroblast-macrophage communication was present in the dermis of psoriasis lesions, exacerbating psoriasis progression. A natural product library was used to screen for a small molecule compound, celastrol, that could interfere with fibroblast-macrophage communication. It was demonstrated that celastrol targeted low-denisity lipoprotein receptor-related protein 1 (LRP1) to inhibit fibroblast secretion of CCL2 and inhibited psoriasis progression by reducing its recruitment to macrophages, thereby blocking communication between the two cells. Moreover, conditional knockdown of LRP1 by fibroblasts significantly improved psoriasis in mice, suggesting that LRP1 may be an important target for the treatment of psoriasis.

2024-03-31 | GSE230842 | GEO

Cultured cardiomyocytes treated with hyaluronan

Project description:Investigation of the role of hyaluronan in cardiomyocytes . The aims of the study were to determine if cardiomyocytes are capable of detecting hyaluronan and if then intrecellular signaling causes changes in gene expression. The study showed that cardiomyocytes can bind hyaluronan with following change in gene expression.

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Chromatin Remodeling Drives Immune-Fibroblast Cell Communication in Heart Failure

Project description:Chromatin Remodeling Drives Immune-Fibroblast Cell Communication in Heart Failure

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Celastrol targets LRP1 to inhibit fibroblast-macrophage crosstalk and ameliorates psoriasis progression

Project description:Purpose: This study aimed to explore the mechanism of Celastrol in improving psoriasis through single-cell transcriptomics Methods: Supplementation with intragastric administration of celastrol in C57BL/6 mice to observe its effect on IMQ-induced psoriasis. Single-cell RNA sequencing were performed to explore the role of celastrol for IMQ-induced psoriasis. Results: A natural product library was used to screen for a small molecule compound, celastrol, that could interfere with fibroblast-macrophage communication. It was demonstrated that celastrol targeted low-denisity lipoprotein receptor-related protein 1 (LRP1) to inhibit fibroblast secretion of CCL2 and inhibited psoriasis progression by reducing its recruitment to macrophages, thereby blocking communication between the two cells Conclusion: We report that celastrol targeted low-denisity lipoprotein receptor-related protein 1 (LRP1) to inhibit fibroblast secretion of CCL2 and inhibited psoriasis progression by reducing its recruitment to macrophages. The use of celastrol maybe a noveltherapeuticoption for psoriasis.

2024-04-20 | GSE231728 | GEO

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Project description:Chronic inflammation and tissue fibrosis are common stress responses that worsen organ function, yet their crosstalk is poorly understood. Here, we show that conditional deletion of the transcription co-activator Brd4 in Cx3cr1-positive myeloid cells ameliorates heart failure and is associated with a dramatic reduction in fibroblast activation. We identified a specific BRD4-occupied enhancer in Cx3cr1-positive cells that controls expression of Interleukin-1 beta (Il1b), and show that secreted IL1B activates a p65/RELA-dependent enhancer downstream of MEOX1, driving a profibrotic response in human cardiac fibroblasts. In vivo, antibody-mediated IL1B neutralization prevented stress-induced expression of MEOX1, inhibited fibroblast activation, and improved cardiac function in heart failure. The elucidation of BRD4-dependent crosstalk between a specific immune cell subset and fibroblasts through IL1B provides new therapeutic strategies for heart disease and other disorders of chronic inflammation and maladaptive tissue remodeling.

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