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Spatial Transcriptomics Unravels Palmitoylation and Zonation-Dependent Gene Regulation by AEG-1 in Mouse Liver

ABSTRACT: Spatial Transcriptomics Unravels Palmitoylation and Zonation-Dependent Gene Regulation by AEG-1 in Mouse Liver

PROVIDER: PRJNA1085111 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28254633_1.fastq.gz	Fastqsanger.gz
	SRR28254633_2.fastq.gz	Fastqsanger.gz
	SRR28254634_1.fastq.gz	Fastqsanger.gz
	SRR28254634_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

Spatial Transcriptomics Unravels Palmitoylation and Zonation-Dependent Gene Regulation by AEG-1 in Mouse Liver

Project description:Obesity-induced metabolic dysfunction-associated steatohepatitis (MASH) leads to hepatocellular carcinoma (HCC). Astrocyte-elevated gene-1/Metadherin (AEG-1/MTDH) plays a key role in promoting MASH and HCC. AEG-1 is palmitoylated at residue cysteine 75 (Cys75) and a knock-in mouse representing mutated Cys75 to serine (AEG-1-C75S) showed activation of MASH- and HCC-promoting gene signature when compared to wild-type littermates (AEG-1-WT). The liver consists of 3 zones, periportal, midlobular and pericentral, and zone-specific dysregulated gene expression impairs metabolic homeostasis in the liver, contributing to MASH and HCC. Here, to elucidate how palmitoylation influences AEG-1-mediated gene regulation in regards to hepatic zonation, we performed spatial transcriptomics (ST) in the livers of AEG-1-WT and AEG-1-C75S littermates.

2024-06-05 | GSE261057 | GEO

Palmitoylation negatively regulates AEG-1 function

Project description:In vitro studies revealed that AEG-1 is palmitoylated at cysteine at a.a. 75 position. In order to check how palmitoylation regulates AEG-1 function in vivo we generated a knockin moue using CRISPR/Cas9 taking in which cysteine 75 was mutated to serine (AEG-1-C75S). Hepatocytes were isolated from AEG-1-WT and AEG-1C75S littermates, total RNA was isolated and RNA-sequencing was performed.

2023-01-25 | GSE215113 | GEO

Palmitoylation negatively regulates AEG-1 function

Project description:Palmitoylation negatively regulates AEG-1 function

| PRJNA888790 | ENA

Spatial Transcriptomics to define transcriptional patterns of zonation and structural components in the liver

Project description:Reconstruction of heterogeneity through single-cell transcriptional profiling has greatly advanced our understanding of the spatial liver transcriptome in recent years. However, global transcriptional differences across lobular units remain elusive in physical space. Here, we implement Spatial Transcriptomics to perform transcriptomic analysis across sectioned liver tissue. We confirm that the heterogeneity in this complex tissue is predominantly determined by lobular zonation. By introducing novel computational approaches, we enable transcriptional gradient measurements between tissue structures, including several lobules in a variety of orientations. Further, our data suggests the presence of previously transcriptionally uncharacterized structures within liver tissue, contributing to the overall spatial heterogeneity of the organ. This study demonstrates how comprehensive spatial transcriptomic technologies can be used to delineate extensive spatial gene expression patterns in the liver, indicating its future impact for studies of liver function, development and regeneration as well as its potential in pre-clinical and clinical pathology. Additional data to reproduce the data presented in this study with instrctions can be found at https://github.com/almaan/ST-mLiver and https://zenodo.org/record/4399655

2021-01-20 | GSE165141 | GEO

Single-cell transcriptomics uncovers zonation of function in the mesenchyme during liver fibrosis

Project description:We profile the transcriptomes of ~30,000 mouse single cells to deconvolve the hepatic mesenchyme in healthy and fibrotic liver at high resolution. We reveal spatial zonation of hepatic stellate cells across the liver lobule, designated portal vein-associated HSC and central vein-associated HSC, and uncover an equivalent functional zonation in a mouse model of centrilobular fibrosis. Our work illustrates the power of single-cell transcriptomics to resolve key collagen-producing cells driving liver fibrosis with high precision.

2019-11-01 | GSE137720 | GEO

Perturbed liver gene zonation in a mouse model of non-alcoholic steatohepatitis

Project description:Liver zonation characterizes the separation of metabolic pathways along the lobules and is required for optimal hepatic function. Wnt signaling is a master regulator of spatial liver zonation. A perivenous-periportal Wnt activity gradient orchestrates metabolic zonation by activating genes in perivenous hepatocytes, while suppressing genes in their periportal counterparts. The understanding of liver gene zonation and zonation regulators in disease was limited. Non-alcoholic steatohepatitis (NASH) is a chronic liver disease characterized by fat accumulation, inflammation, and fibrosis. Here, we investigated the perturbation of liver gene zonation in a mouse NASH model by combination of spatial transcriptomics, bulk RNAseq and in situ hybridization. Wnt target genes represented a major subset of genes showing altered spatial expression in the NASH liver. The altered Wnt target gene expression level and zonation spatial pattern were in line with the upregulation of Wnt regulators and the augmentation of Wnt signaling. Particularly, we found that the Wnt activator Rspo3 expression was restricted to the perivenous zone in control livers, whereas expanded to the periportal zone in NASH livers. AAV8-mediated RSPO3 overexpression in controls resulted in a zonation change, and further amplified the disturbed zonation of Wnt target genes in NASH, but had no impacts on steatosis, inflammation and fibrosis. In summary, our study demonstrated the alteration of Wnt signaling in a mouse NASH model, leading to perturbed liver zonation.

2024-08-01 | GSE248077 | GEO

Spatial Transcriptomics to define transcriptional patterns of zonation and structural components in the liver

Project description:Spatial Transcriptomics to define transcriptional patterns of zonation and structural components in the liver

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The spatial zonation of the placental vasculature is specified by epigenetic mechanisms

Project description:The labyrinthian fetoplacental capillary network is of vital importance for proper nourishment of the developing embryo. An inadequate function of the maternal-fetal circulation has emerged as one of the primary causes of placental insufficiency. Here, we show that the spatial zonation of the placental labyrinth vasculature is controlled by flow-regulated epigenetic mechanisms. The spatial and temporal analysis of gene transcription revealed a gradual change in the expression of epigenetic enzymes with the de novo DNA methyltransferase 3a (DNMT3A) as primary enzyme introducing DNA methylation in cells of the vascular system. Loss of Dnmt3a resulted in DNA hypomethylation and disturbance of the spatial-zonated placental gene expression. The resulting global DNA hypomethylation impaired the angiogenic capacity of endothelial cells. Global as well as endothelium-predominant deletion of Dnmt3a resulted in impaired placental vascularization and fetal growth retardation. A meta-analysis of human placental endothelial cell gene expression identified an association between preeclampsia and reduction of DNMT3A. Collectively, our study identified DMNT3A as critical methylome-regulator of placental endothelial cell gene expression and function with clinical implications for the pathogenesis of placental dysfunction, as it occurs during preeclampsia or fetal growth retardation.

2024-11-21 | GSE280168 | GEO

Spatial Transcriptomics of ageing mouse liver tissues give insights into the zonation-specific lipid deposition

Project description:Spatial Transcriptomics of ageing mouse liver tissues give insights into the zonation-specific lipid deposition

| PRJEB60699 | ENA

Dose-dependent disruption of hepatic zonation by 2,3,7,8-tetrachlorodibenzo-p-dioxin in mice: integration of single-nuclei RNA sequencing and spatial transcriptomics

Project description:2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) dose-dependently induces the development of hepatic fat accumulation and inflammation with fibrosis in mice initially in the portal region. Conversely, differential gene and protein expression is first detected in the central region. To further investigate cell-specific and spatially resolved dose-dependent changes in gene expression elicited by TCDD, single-nuclei RNA sequencing and spatial transcriptomics were used for livers of male mice gavaged with TCDD every 4 days for 28 days. The proportion of 11 cell (sub)types across 131,613 nuclei dose-dependently changed with 68% of all portal and central hepatocyte nuclei in control mice being overtaken by macrophages following TCDD treatment. We identified 368 (portal fibroblasts) to 1,339 (macrophages) differentially expressed genes. Spatial analyses revealed initial loss of portal identity that eventually spanned the entire liver lobule with increasing dose. Induction of R-spondin 3 (Rspo3) and pericentral Apc, suggested dysregulation of the Wnt/β-catenin signaling cascade in zonally resolved steatosis. Collectively, the integrated results suggest disruption of zonation contributes to the pattern of TCDD-elicited NAFLD pathologies.

2022-10-21 | GSE206294 | GEO

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