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Resolvin D1 attenuated liver injury caused by chronic ethanol and acute LPS challenge in mice

ABSTRACT: Resolvin D1 attenuated liver injury caused by chronic ethanol and acute LPS challenge in mice

PROVIDER: PRJNA910124 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22575310_1.fastq.gz	Fastqsanger.gz
	SRR22575310_2.fastq.gz	Fastqsanger.gz
	SRR22575311_1.fastq.gz	Fastqsanger.gz
	SRR22575311_2.fastq.gz	Fastqsanger.gz
	SRR22575312_1.fastq.gz	Fastqsanger.gz

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Resolvin D1 attenuated liver injury caused by chronic ethanol and acute LPS challenge in mice

Project description:Alcohol-associated liver disease (ALD) is a major health problem with limited effective treatment options. Alcohol-associated hepatitis (AH) is a subset of severe ALD with a high rate of mortality due to infection, severe inflammation, and ultimately multi-organ failure. There is an urgent need for novel therapeutic approaches to alleviate the human suffering associated with this condition. Resolvin D1 (RvD1) promotes the resolution of inflammation and regulates immune responses. The current study aimed to test the therapeutic efficacy and mechanisms of RvD1-mediated effects on liver injury and inflammation in an experimental animal model that mimics severe AH in humans. Our data demonstrated that mice treated with RvD1 had attenuated liver injury and inflammation caused by EtOH and LPS exposure by limiting hepatic neutrophil accumulation and decreasing hepatic levels of pro-inflammatory cytokines. In addition, RvD1 treatment attenuated hepatic pyroptosis, an inflammatory form of cell death, via downregulation of pyroptosis-related genes such as GTPase family member b10 and guanylate binding protein 2, and reducing cleavage of caspase 11 and gasdermin-D. In vitro experiments with primary mouse hepatocytes and bone marrow-derived macrophages confirmed the effectiveness of RvD1 in the attenuation of pyroptosis. In summary, our data demonstrated that RvD1 treatment provided beneficial effects against liver injury and inflammation in an experimental animal model recapitulating features of severe AH in humans. Our results suggest that RvD1 may be a novel adjunct strategy to traditional therapeutic options for AH patients.

2023-09-05 | GSE220520 | GEO

Resolvin D1 improves allograft osteointegration and directly enhances osteoblasts differentiation

Project description:Resolvin D1 improves allograft osteointegration and directly enhances osteoblasts differentiation

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Resolvin D1 attenuated liver injury caused by chronic ethanol and acute LPS challenge in mice.

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Gene expression profile at single cell level of leukocytes from transplanted syngeneic left lung grafts following treatment with Resolvin D1.

Project description:Neutrophils play a pivotal role in the pathogenesis of lung ischemia-reperfusion injury. The effect of pro-resolving lipid mediators, such as Resolvin D1, on early neutrophil trafficking has not been assessed in organ transplantation. We obtained single-cell RNA sequencing of leukocytes from syngeneic left lung grafts to elucidate the genetic changes induced by recipient treatment with Resolvin D1 or vehicle.

2023-07-15 | GSE237110 | GEO

Resolvin D1 improves allograft osteointegration and directly enhances osteoblasts differentiation

Project description:Resolvin D1 improves allograft osteointegration and directly enhances osteoblasts differentiation

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Resolvin D1–mediated cellular crosstalk protects against MASH [scRNA-seq]

Project description:Resolvin D1–mediated cellular crosstalk protects against MASH [scRNA-seq]

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Resolvin D1–mediated cellular crosstalk protects against MASH [Bulk RNA-seq]

Project description:Resolvin D1–mediated cellular crosstalk protects against MASH [Bulk RNA-seq]

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Resolvin D1–mediated cellular crosstalk protects against MASH [scRNA-seq]

Project description:Recent studies have highlighted the beneficial effect of resolvin D1 (RvD1), a DHA-derived specialized pro-resolving mediator, on metabolic dysfunction-associated steatohepatitis (MASH), but the underlying mechanisms are not well understood. Our study aims to determine the mechanism by which RvD1 protects against MASH progression. RvD1 was administrated to MASH mice, followed by bulk and single-cell RNA sequencing analysis. Primary cells including bone marrow-derived macrophages (BMDMs), Kupffer cells, T cells, and primary hepatocytes were isolated to study the effect of RvD1 on inflammation, cell death, and fibrosis regression genes. RvD1 administration improved MASH features including reducing inflammation, cell death, and liver fibrosis. Mechanistically, RvD1 reduced inflammation by suppressing the stat1-cxcl10 signaling pathway in macrophages and prevented cell death by alleviating ER stress-mediated apoptosis in hepatocytes. Moreover, RvD1 induced Mmp2 and decreased Acta2 expression in hepatic stellate cells (HSCs), and promoted Mmp9 and Mmp12 expression in macrophages, leading to fibrosis regression in MASH. RvD1 reduced stat1-mediated pro-inflammatory response, mitigated ER stress-induced apoptosis, and promotes MMP-mediated fibrosis regression in MASH. Thus, our study highlights the therapeutic potential of RvD1 for MASH.

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p38 Mitogen-Activated Protein Kinase Signals the Immunoresolving Actions of Resolvin D1 in Inflamed Human Visceral Adipose Tissue

Project description:Activation of the innate immune system leading to a persistent state of low-grade of tissue inflammation greatly influences the risk of developing metabolic complications associated with obesity. In this study, we characterized the inflammatory state in adipose tissue from obese patients and explored the potential of the specialized pro-resolving mediator (SPM) resolvin D1 (RvD1) to actively terminate inflammation and promote its resolution. By means of high-troughput transcritomic analysis we identified a cytokine-related molecular signature in obese omental adipose tissue, characterized by a remarkable overexpression of interleukin (IL)-6, IL-1Î² and IL-10 associated with a concomitant increase in macrophage infiltration, which gradually increased in a body mass index-dependent manner. RNA profiling was conducted in 4 patients with morbid obesity and 4 control subjects using the Affymetrix Human Genome U219 expression array plate containing more than 36,000 transcripts and variants (Affymetrix, Inc., Santa Clara, CA).

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Resolvin D1–mediated cellular crosstalk protects against MASH [Bulk RNA-seq]

2025-04-25 | GSE263768 | GEO