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Transcriptional Dynamics of Hepatic Sinusoid-Associated Cells After Liver Injury [bulk RNA-seq]

ABSTRACT: Transcriptional Dynamics of Hepatic Sinusoid-Associated Cells After Liver Injury [bulk RNA-seq]

PROVIDER: PRJNA1088489 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28357454_1.fastq.gz	Fastqsanger.gz
	SRR28357454_2.fastq.gz	Fastqsanger.gz
	SRR28357455_1.fastq.gz	Fastqsanger.gz
	SRR28357455_2.fastq.gz	Fastqsanger.gz
	SRR28357456_1.fastq.gz	Fastqsanger.gz

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Transcriptional dynamics of hepatic sinusoid-associated cells after liver injury super

Project description:Transcriptional dynamics of hepatic sinusoid-associated cells after liver injury super

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Transcriptional dynamics of hepatic sinusoid-associated cells after liver injury [scRNA-seq]

Project description:Transcriptional dynamics of hepatic sinusoid-associated cells after liver injury [scRNA-seq]

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Hi-C from endothelial cell of hepatic sinusoid (ENCSR982KWR)

Project description:HiC experiment done on endothelial cell of hepatic sinusoid For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf

2017-10-24 | GSE105988 | GEO

Transcriptional Dynamics of Hepatic Sinusoid-Associated Cells After Liver Injury [bulk RNA-seq]

Project description:Here we profile the transcripts of app. 35.000 single cells isolated from livers of healthy and diseased mice. We show the transcriptomic change associated with fibrosis induction in the non-parenchymal cell types (hepatic stellate cells, liver endothelial cells and macrophages). We reveal a hitherto unknown feature of the HSCs otherwise functionally attributed to the LECs.

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Transcriptional dynamics of hepatic sinusoid-associated cells after liver injury [scRNA-seq]

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Transcriptional Dynamics of Hepatic Sinusoid-Associated Cells After Liver Injury.

Project description:Background and aimsHepatic sinusoidal cells are known actors in the fibrogenic response to injury. Activated hepatic stellate cells (HSCs), liver sinusoidal endothelial cells, and Kupffer cells are responsible for sinusoidal capillarization and perisinusoidal matrix deposition, impairing vascular exchange and heightening the risk of advanced fibrosis. While the overall pathogenesis is well understood, functional relations between cellular transitions during fibrogenesis are only beginning to be resolved. At single-cell resolution, we here explored the heterogeneity of individual cell types and dissected their transitions and crosstalk during fibrogenesis.Approach and resultsWe applied single-cell transcriptomics to map the heterogeneity of sinusoid-associated cells in healthy and injured livers and reconstructed the single-lineage HSC trajectory from pericyte to myofibroblast. Stratifying each sinusoidal cell population by activation state, we projected shifts in sinusoidal communication upon injury. Weighted gene correlation network analysis of the HSC trajectory led to the identification of core genes whose expression proved highly predictive of advanced fibrosis in patients with nonalcoholic steatohepatitis (NASH). Among the core members of the injury-repressed gene module, we identified plasmalemma vesicle-associated protein (PLVAP) as a protein amply expressed by mouse and human HSCs. PLVAP expression was suppressed in activated HSCs upon injury and may hence define hitherto unknown roles for HSCs in the regulation of microcirculatory exchange and its breakdown in chronic liver disease.ConclusionsOur study offers a single-cell resolved account of drug-induced injury of the mammalian liver and identifies key genes that may serve important roles in sinusoidal integrity and as markers of advanced fibrosis in human NASH.

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Transcriptional dynamics of hepatic sinusoid-associated cells after liver injury super

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-03-15 | GSE261721 | GEO

Proteomics analysis of different stages during mouse hepatic ischemia-reperfusion injury

Project description:6-plex TMT-based quantitative proteomics was used to analysis the proteomic profile in different stages of mouse hepatic ischemia-reperfusion injury.

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Transcriptional dynamics of hepatic stellate cells in experimental acute liver injury, liver fibrosis and liver fibrosis reversal.

Project description:Transcriptional alterations during different stages of hepatic stellate cell activation were determined using RNA Sequencing. Models include acute liver injury (1 injection of CCl4) and chronic liver injury (8 injections of CCl4 over 4-week period) with different recovery timepoints. Illumina NextSeq 500 High was used for sequencing.

2021-12-15 | GSE176042 | GEO

Hepatic mitochondrial proteome dynamics in NAFLD mice

Project description:Nonalcoholic fatty liver disease (NAFLD) is associated with hepatic mitochondrial dysfunction characterized by reduced ATP synthesis. We applied the 2H2O-metabolic labeling approach to test the hypothesis that the reduced stability of oxidative phosphorylation proteins contributes to mitochondrial dysfunction in a diet-induced mouse model of NAFLD. A high fat diet containing cholesterol (a so-called Western diet (WD)) led to hepatic oxidative stress, steatosis, inflammation and mild fibrosis, all markers of NAFLD, in LDLR-/- mice. In addition, compared to controls, livers from NAFLD mice had reduced citrate synthase activity and ATP content, suggesting reduced mitochondrial oxidative capacity. Proteome dynamics analysis revealed that mitochondrial dysfunction is associated with reduced average half-lives of mitochondrial proteins in NAFLD mice (5.41±0.46 vs. 5.15±0.49 day, P<0.05). In particular, the WD reduced stability of oxidative phosphorylation subunits, including cytochrome c oxidase subunit 4 isoform 1 of complex III (5.9 ± 0.1 vs 3.4 ± 0.8 day), ATP synthase subunit α (6.3±0.4 vs. 5.5±0.4 day) and ATP synthase F(0) complex subunit B1 of complex V (8.5±0.6 vs. 6.5±0.2 day) (P<0.05). These changes were associated with impaired complex III and F0F1-ATP synthase activities, suggesting that increased degradation of mitochondrial proteins contributed to hepatic mitochondrial dysfunction in NAFLD mice. Autophagy, but not proteasomal degradation, contributed to increased clearance of hepatic mitochondrial proteins in NAFLD mice. In conclusion, the proteome dynamics approach suggests that alterations in mitochondrial proteome dynamics is involved in hepatic mitochondrial dysfunction in NAFLD.

2018-11-21 | PXD008766 | Pride

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