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

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

PROVIDER: PRJNA1099213 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28627673_1.fastq.gz	Fastqsanger.gz
	SRR28627673_2.fastq.gz	Fastqsanger.gz
	SRR28627674_1.fastq.gz	Fastqsanger.gz
	SRR28627674_2.fastq.gz	Fastqsanger.gz
	SRR28627675_1.fastq.gz	Fastqsanger.gz

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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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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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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.

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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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Cholesterol-Associated Locus EHBP1 Protects Against MASH Fibrosis

Project description:Cholesterol-Associated Locus EHBP1 Protects Against MASH Fibrosis

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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-1β and IL-10 associated with a concomitant increase in macrophage infiltration, which gradually increased in a body mass index-dependent manner.

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Project description:Excess cholesterol accumulation contributes to fibrogenesis in metabolic dysfunction-associated steatohepatitis (MASH, formerly known as nonalcoholic steatohepatitis [NASH]), but how hepatic cholesterol metabolism becomes dysregulated in MASH is not completely understood. We show here that human fibrotic MASH livers have decreased EHBP1, a novel GWAS locus associated with LDL cholesterol, and that the EHBP1 rs10496099 T>C variant in MASH patients is associated with decreased hepatic EHBP1 expression and with augmented MASH fibrosis. Congruent with the human data, EHBP1 loss- and gain-of-function increases and decreases MASH fibrosis in mice, respectively. Mechanistic studies reveal that EHBP1 promotes sortilin (SORT1)-mediated PCSK9 secretion, leading to LDLR degradation, decreased LDL uptake, and reduced TAZ, a fibrogenic effector. At a cellular level, EHBP1 deficiency affects intracellular localization of retromer, a protein complex required for sortilin stabilization. Our novel therapeutic approach to stabilizing retromer is effective in mitigating MASH fibrosis. Moreover, we show that the TNFα/PPARα pathway suppresses EHBP1 in MASH. These data not only provide new mechanistic insight into the role of EHBP1 in cholesterol metabolism and MASH fibrosis by uncovering the interaction between EHBP1 and other cholesterol-related loci, including SORT1, PCSK9, and LDLR, but also elucidate a novel interplay between inflammation and EHBP1-mediated cholesterol metabolism.

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