Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hepatocyte-derived Pumilio1-enriched exosomes inhibit hepatic stellate cell activation by suppressing tropomyosin-4 translation

ABSTRACT: Hepatocyte-derived Pumilio1-enriched exosomes inhibit hepatic stellate cell activation by suppressing tropomyosin-4 translation

PROVIDER: PRJNA1254274 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR33259239_1.fastq.gz	Fastqsanger.gz
	SRR33259239_2.fastq.gz	Fastqsanger.gz
	SRR33259240_1.fastq.gz	Fastqsanger.gz
	SRR33259240_2.fastq.gz	Fastqsanger.gz
	SRR33259241_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Hepatocyte-derived Pumilio1-enriched exosomes inhibit hepatic stellate cell activation by suppressing tropomyosin-4 translation

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD) has become the most common chronic liver disease globally. Abnormal crosstalk between hepatocytes and hepatic stellate cells (HSCs) leads to liver fibrosis and aggravates MASLD. We explored the role of the RNA-binding protein Pumilio in this process.

2025-04-27 | GSE295362 | GEO

miR-182-5p Promotes Hepatocyte-Stellate Cell Crosstalk to Facilitate Liver Regeneration

Project description:A unique feature of the liver is its high regenerative capacity, which is essential to maintain liver homeostasis. However, key regulators of liver regeneration (LR) remain ill-defined. Here, we identify hepatic miR-182-5p as a key regulator of LR. Suppressing miR-182-5p, whose expression is significantly induced in the liver of mice post two-thirds partial hepatectomy (PH), abrogates PH-induced LR in mice. In contrast, liver-specific overexpression of miR-182-5p promotes LR in mice with PH. Overexpression of miR-182-5p failed to promote proliferation in hepatocytes, but stimulates proliferation when hepatocytes are cocultured with stellate cells. Mechanistically, miR-182-5p stimulates Cyp7a1-mediated cholic acid production in hepatocytes, which promotes hedgehog (Hh) ligand production in stellate cells, leading to the activation of Hh signaling in hepatocytes and consequent cell proliferation. Collectively, our study identified miR-182-5p as a critical regulator of LR and uncovers a Cyp7a1/cholic acid-dependent mechanism by which hepatocytes crosstalk to stellate cells to facilitate LR.

2022-08-10 | GSE206451 | GEO

Hepatic stellate cells maintain liver homeostasis through paracrine neurotrophin-3 signaling that induces hepatocyte proliferation

Project description:Organ size is maintained by the controlled proliferation of distinct cell populations. In the mouse liver, hepatocytes in the midlobular zone that are positive for cyclin D1 (CCND1) repopulate the parenchyma at a constant rate to preserve liver mass. Here, we investigated how hepatocyte proliferation is supported by hepatic stellate cells (HSCs), pericytes that are in close proximity to hepatocytes. We used T cells to ablate nearly all HSCs in the murine liver, enabling the unbiased characterization of HSC functions. In the normal liver, complete loss of HSCs persisted for up to 10 weeks and caused a gradual reduction in liver mass and in the number of CCND1+ hepatocytes. We identified neurotrophin-3 (Ntf-3) as an HSC-produced factor that induced the proliferation of midlobular hepatocytes through the activation of tropomyosin receptor kinase B (TrkB). Treating HSC-depleted mice with Ntf-3 restored CCND1+ hepatocytes in the midlobular region and increased liver mass. These findings establish that HSCs form the mitogenic niche for midlobular hepatocytes and identify Ntf-3 as a hepatocyte growth factor.

2023-06-27 | GSE211370 | GEO

Genome-wide analysis of adipose tissue from cytoskeletal tropomyosin transgenic mice

2015-06-21 | GSE25013 | GEO

Genome-wide analysis of adipose tissue from cytoskeletal tropomyosin transgenic mice

Project description:Analysis of the effect on global gene regulation in epididymal adipose tissue of overexpressing the cytoskeletal tropomyosin, Tm5NM1 to help understand the transcriptional events that lead to increased fat mass in transgenic mice. Total RNA obtained from epididymal adipose tissue for 3 month old transgenic and non-transgenic control mice.

2015-06-21 | E-GEOD-25013 | biostudies-arrayexpress

Tropomyosin 1 deficiency facilitates cell state transitions and enhances hemogenic endothelial cell specification during hematopoiesis

Project description:The goal of this study was to determine the developmental stage(s) and mechanisms by which Tropomyosin 1 impacts hematopoiesis.

2023-10-02 | GSE244112 | GEO

The effect of postoperative stellate ganglion block on myocardial injury in patients undergoing laparoscopic radical resection of colorectal cancer

Project description:Interventions: Block Group:Stellate ganglion block;Routine Group:Saline injection around the stellate ganglion Primary outcome(s): Troponin I Study Design: Parallel

| 35777 | ecrin-mdr-crc

The purinergic P2Y14 receptor links hepatocyte death to hepatic stellate cell activation and fibrogenesis in the liver

Project description:Characterization of hepatic stellate cells (HSC) genes in the normal liver or diverse liver fibrotic models by single cell RNA sequencing.

2022-04-07 | GSE172492 | GEO

An imbalance of tumour-suppressing and tumour-promoting hepatic stellate cell populations in liver fibrosis contributes to hepatocarcinogenesis

Project description:An imbalance of tumour-suppressing and tumour-promoting hepatic stellate cell populations in liver fibrosis contributes to hepatocarcinogenesis

| PRJNA731458 | ENA

Lysine acetylation of F-actin decreases tropomyosin-based inhibition of actomyosin activity

Project description:Actin was acetylated on lysine residues with acetic anhydride to determine its impaction on the contractile properties of the thin filaments including, actin's ability to undergo crossbridge cycling with myosin, actin's affinity for tropomyosin, and the impact of actin acetylation on calcium regulated thin filament activation

2020-09-04 | PXD020732 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data