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Gene expression profile at single cell level of hepatocytes and non parenchymal cells (NPCs) isolated from a murine model of MASLD

ABSTRACT: Gene expression profile at single cell level of hepatocytes and non parenchymal cells (NPCs) isolated from a murine model of MASLD

PROVIDER: PRJNA1197525 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31700381_1.fastq.gz	Fastqsanger.gz
	SRR31700381_2.fastq.gz	Fastqsanger.gz
	SRR31700382_1.fastq.gz	Fastqsanger.gz
	SRR31700382_2.fastq.gz	Fastqsanger.gz
	SRR31700383_1.fastq.gz	Fastqsanger.gz

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Gene expression profile at single cell level of hepatocytes and non parenchymal cells (NPCs) isolated from a murine model of MASLD

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD) embraces different conditions, including metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, cirrhosis and hepatocellular carcinoma (HCC). The landscape of cellular abnormalities occurring in the different stages of MASLD as well as the processes which drive MASLD evolution are not completely clarified. We used single cell RNAsequencing (scRNAseq) to unravel cellular heterogeneity affecting livers during the switching from simple steatosis towads MASH and and MASH-fibrosis.

2025-02-28 | GSE284186 | GEO

The Senescence-associated Secretome of Hedgehog-deficient Hepatocytes Drives MASLD Progression

Project description:The burden of senescent hepatocytes correlates with MASLD severity but mechanisms driving senescence, and how it exacerbates MASLD are poorly understood. Hepatocytes become senescent when Smoothened (Smo) is deleted to disrupt Hedgehog signaling. We aimed to determine if the secretomes of Smo-deficient hepatocytes perpetuate senescence to drive MASLD progression. RNA seq analysis confirmed that hepatocyte populations of MASLD livers are depleted of Smo(+) cells and enriched with senescent cells. When fed CDA-HFD, Smo(-) mice had lower antioxidant markers and developed worse DNA damage, senescence, MASH and liver fibrosis than Smo(+) mice. Sera and hepatocyte-conditioned medium from Smo(-) mice were depleted of thymidine phosphorylase (TP), a protein that maintains mitochondrial fitness. Treating Smo(-) hepatocytes with TP reduced senescence and lipotoxicity; inhibiting TP in Smo(+) hepatocytes had the opposite effects and exacerbated hepatocyte senescence, MASH, and fibrosis in CDA-HFD-fed mice.Therefore, we found that inhibiting Hedgehog signaling in hepatocytes promotes MASLD by suppressing hepatocyte production of proteins that prevent lipotoxicity and senescence.

2024-10-01 | GSE273523 | GEO

Bulk RNA sequencing analysis of hepatocytes isolated from humanized liver

Project description:The goal of this experiment was to identify differentially expressed human genes in the hepatocyte fraction between two groups. Group A includes mice having only human hepatocytes and group B includes mice having both human hepatocytes and human Non-Parenchymal Cells (NPCs).

2023-06-16 | GSE234757 | GEO

Single cell qRT-PCR (scPCR) for rat hepatocytes and biliary epithelial cell (BEC)-enriched non-parenchymal cells (NPCs).

Project description:Using FACS-sorted adult rat hepatocytes with distinct DNA contents (2c and 4c), we compared the expression levels of a 47 gene panel. As non-hepatic control samples, BEC-enriched NPCs were also used for the same scPCR experiment.

2019-08-01 | GSE132459 | GEO

Adult hepatocytes direct liver organogenesis through non-parenchymal cell recruitment in the kidney

Project description:Background & Aims: Since the first account of the myth of Prometheus, the amazing regenerative capacity of the liver has fascinated researchers due to its enormous medical potential. Liver regeneration is promoted by multiple types of liver cells, including hepatocytes and liver non-parenchymal cells (NPCs), through the complex intercellular signaling. However, the liver organogenetic mechanism, especially the role of adult hepatocytes at ectopic sites, remains unknown. In this study, we demonstrate that hepatocytes alone spurred liver organogenesis to form an organ-sized complex 3D liver that exhibited native liver architecture and functions in the kidneys of mice. Methods: Isolated hepatocytes were transplanted under the kidney capsule of monocrotaline (MCT) and partial hepatectomy (PHx)-treated mice. To determine the origin of NPCs in neo-livers, hepatocytes were transplanted into MCT/PHx-treated green fluorescent protein (GFP) transgenic mice or wild-type mice transplanted with bone marrow (BM) cells isolated from GFP mice. Results: Hepatocytes engrafted at the subrenal space of mice underwent continuous growth in response to a chronic hepatic injury in the native liver. More than 1.5 yrs later, whole organ-sized liver tissues having a greater mass than those of the injured native liver had formed. Most remarkably, we revealed that at least three types of NPCs with similar phenotypic features to the liver NPCs were recruited from the host tissues including BM. The neo-livers in the kidney exhibited liver-specific functions and architectures, including sinusoidal vascular systems, zonal heterogeneity, and emergence of bile duct cells. Furthermore, the neo-livers successfully rescued the mice with lethal liver injury. Conclusion: Our data clearly showed that adult hepatocytes play a leading role as organizer cells in liver organogenesis at ectopic sites via NPC recruitment.

2017-12-25 | GSE99141 | GEO

Single cell qRT-PCR (scPCR) for rat hepatocytes and biliary epithelial cell (BEC)-enriched non-parenchymal cells (NPCs).

Project description:Single cell qRT-PCR (scPCR) for rat hepatocytes and biliary epithelial cell (BEC)-enriched non-parenchymal cells (NPCs).

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Transcription profiling of mouse with txnrd1 specifically disrupted in all parenchymal hepatocytes - reveals cytoprotective Nrf2 pathway is induced in chronically Txnrd1-deficient hepatocytes

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2009-06-24 | E-GEOD-16381 | biostudies-arrayexpress

The Senescence-associated Secretome of Hedgehog-deficient Hepatocytes Drives MASLD Progression

Project description:The Senescence-associated Secretome of Hedgehog-deficient Hepatocytes Drives MASLD Progression

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Targeting Senescent Hepatocytes for Treatment of Metabolic Dysfunction-associated Steatotic Liver Disease and Multi-organ Dysfunction

Project description:Senescent hepatocytes accumulate in metabolic dysfunction-associated steatotic liver disease (MASLD) and are linked to worse clinical outcomes. However, their heterogeneity and lack of specific markers have made them difficult to target therapeutically. Here, we define a senescent hepatocyte gene signature (SHGS) using in vitro and in vivo models and show that it tracks with MASLD progression/regression across mouse models and large human cohorts. Single-nucleus RNA-sequencing and functional studies reveal that SHGS+ hepatocytes originate from p21+ cells, lose key liver functions and release factors that drive disease progression. One such factor, GDF15, increases in circulation alongside SHGS+ burden and disease progression. Through chemical screening, we identify senolytics that selectively eliminate SHGS+ hepatocytes and improve MASLD in mice. Notably, SHGS enrichment also correlates with dysfunction in other organs. These findings establish SHGS+ hepatocytes as key drivers of MASLD and highlight a potential therapeutic strategy for targeting senescent cells in liver disease and beyond.

2025-02-21 | GSE288534 | GEO

A Single-Cell Atlas of Murine Liver Non-parenchymal Cells in Typical Disease Models

Project description:We provided a comprehensive single-cell transcriptomic atlas of murine liver non-parenchymal cells (NPCs) in different diseases and analyzed the heterogeneity of inter- and intra-group NPCs. Our study offers a valuable resource for better understanding liver physiology and pathology, and bring new directions for the development of clinical diagnostic markers and effective therapeutic targets.

2021-08-01 | GSE166178 | GEO

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