Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SnRNA-seq Analysis of Sox9f/f and Sox9HKO Mouse Liver Transcriptomes

ABSTRACT: Purpose: To identify the alterations of genes transcriptional profile of livers obtained from Sox9f/f mice and Sox9HKO mice treated with partial hepatectomy (PHx). Methods: Sox9HKO mice were generated by Sox9f/f mice injected with AAV-TBG-Cre via tail. Sox9f/f mice and Sox9HKO mice were treated with PHx to induce liver regeneration. Liver mRNA profiles of 12-week-old Sox9f/f and Sox9HKO mice treated with PHx were generated by deep sequencing, using 10 × library preparation, each cDNA molecule was tagged on the 3’end of a mRNA transcript with unique molecular identifiers (UMI) and cell labels indicating its cell of origin on cDNA synthesis. We applied DESeq2 algorithm to filter the differentially expressed genes, after the significant analysis and FDR analysis under the following criteria: i) |log2FC| > 1 ; ii) Pvalue < 0.05. Results: We identified the transcripts in the livers of Sox9f/f and Sox9HKO mice and identified the differential expression between Sox9f/f and Sox9HKO mouse hepatocytes, with a |log2FC| > 1 and P value < 0.05. Conclusion: Our study represents the first detailed analysis of liver transcriptomes of Sox9HKO mice during liver regeneration. snRNA-seq based transcriptome analysis would provide us with a better understanding of the complex biological functions of Sox9 in the hepatocyte during the process of hepatocyte proliferation in mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE278895 | GEO | 2025/11/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-seq Analysis of Sox9f/f and Sox9HKO Mouse Primary Hepatocyte Transcriptomes

Project description:Purpose: To identify the alterations of genes transcriptional profile of hepatocytes obtained from Sox9f/f mice and Sox9HKO mice treated with partial hepatectomy (PHx). Methods: Sox9HKO mice were generated by Sox9f/f mice injected with AAV-TBG-Cre via tail. Sox9f/f mice and Sox9HKO mice were treated with PHx to induce liver regeneration. Liver mRNA profiles of 12-week-old Sox9f/f and Sox9HKO mice treated with PHx were generated by deep sequencing, using Illumina Novaseq 6000. We applied DESeq2 algorithm to filter the differentially expressed genes, after the significant analysis and FDR analysis under the following criteria: i) |log2FC| > 1 ; ii) Pvalue < 0.05. RT–PCR validation was performed using SYBR Green PCR Kit. Results: We identified the transcripts in the hepatocytes of Sox9f/f and Sox9HKO mice. 1379 transcripts showed differential expression between Sox9f/f and Sox9HKO mouse hepatocytes, with a |log2FC| > 1 and P value < 0.05. Altered expression of 4 genes was confirmed by qRT–PCR. Conclusion: Our study represents the first detailed analysis of liver transcriptomes of Sox9HKO mice during liver regeneration. RNA-seq based transcriptome analysis would provide us with a better understanding of the complex biologic functions of Sox9 in the hepatocyte during the pricess of hepatocyte proliferation in mice.

2025-11-25 | GSE278894 | GEO

Survivin deficient liver of mice after partial hepatectomy

Project description:The liver possesses remarkable regenerative capacity in response to injury. Upon partial hepatectomy (PHx), terminally differentiated hepatocytes in the remaining liver enter the cell cycle and restore the liver mass and function within weeks. However, liver regeneration is often impaired in livers with chronic diseases. Survivin, an inhibitor of apoptosis protein (IAP) and member of chromosome passenger complex (CPC), plays versatile roles in cell mitosis and apoptosis. We and others found that the expression of Survivin was highly increased in liver during PHx-induced liver regeneration, which indicated that Survivin played important roles in this process. However, the function of Survivin in liver regeneration remains largely undefined. Here, using mice with genetic deletion of Survivin, we found that during PHx-induced liver regeneration Survivin regulated both hepatocyte G1/S phase transition by inhibiting the expression of p21 and G2/M phase transition by regulating the localization of CPC. Moreover, restoration of Survivin expression in Survivin-deficient hepatocytes inhibited p21 expression and promote both hepatocyte G1/S and G2/M transition during PHx-induced liver regeneration.

2017-01-01 | GSE83598 | GEO

Spatiotemporal expression of HMGB2 regulates cell proliferation and hepatocyte size during liver regeneration

Project description:Liver regeneration is an extraordinarily complex process involving a variety of factors; however, the role of chromatin protein in hepatocyte proliferation is largely unknown. In this study, we investigated the functional role of high-mobility group box 2 (HMGB2), a chromatin protein in liver regeneration using wild-type and HMGB2-knockout (KO) mice. Liver tissues were sampled after 70% partial hepatectomy (PHx), and analyzed by immunohistochemistry using various markers of cell proliferation, including Ki-67, PCNA, cyclin D1, cyclin B1, EdU and pH3S10. In WT mice, hepatocyte proliferation was strongly correlated with the spatiotemporal expression of HMGB2; however, cell proliferation was significantly delayed in hepatocytes of HMGB2-KO mice. Quantitative PCR demonstrated that cyclin D1 and cyclin B1 mRNAs were significantly decreased in HMGB2-KO mice livers. Interestingly, hepatocyte size was significantly larger in HMGB2-KO mice at 36-72 h after PHx, and these results suggest that hepatocyte hypertrophy appeared in parallel with delayed cell proliferation. In vitro experiments demonstrated that cell proliferation was significantly decreased in HMGB2-KO cells. A significant delay in cell proliferation was also found in HMGB2-siRNA transfected cells. In summary, spatiotemporal expression of HMGB2 is important for regulation of hepatocyte proliferation and cell size during liver regeneration.

2022-04-03 | GSE199944 | GEO

Aquaporin 5 deficiency suppresses fatty acid oxidation and delays liver regeneration through the transcription factor PPAR.

Project description:After 70% partial hepatectomy (PHx), the metabolic pathways leading to hepatocyte lipid droplet accumulation during liver regeneration remain unclear. Aquaporin 5 (Aqp5) is an aquaporin and peroporin that facilitates the transport of both water and hydrogen peroxide (H2O2). In this study, we observed a delayed liver regeneration following PHx in Aqp5 knockout (Aqp5−/−) mice. Considering the role of Aqp5 in H2O2 transport, we hypothesized that deficiency in Aqp5 may induce oxidative stress and hepatocyte injury. Through the measurement of reactive oxygen species (ROS) and redox-related indices, we observed significant alterations in ROS levels as well as malondialdehyde (MDA), superoxide dismutase (SOD), and reduced glutathione (GSH) concentrations in regenerating livers lacking Aqp5 compared to wild-type controls. Oil Red O and 4-hydroxynonenal (4-HNE) staining results indicated that Aqp5 deficiency caused lipid accumulation during liver regeneration. The transcriptome sequencing results showed that the PPAR pathway is inhibited during the liver regeneration process in Aqp5 gene-knockout mice.The administration of the WY-14643 agonist, which targets the PPAR pathway, significantly mitigated delayed liver regeneration by enhancing hepatocyte proliferation and reducing lipid accumulation caused by Aqp5 deficiency. Our findings highlight the crucial role of Aqp5 in regulating H2O2 levels and lipid metabolism through the PPAR pathway during liver regeneration.

2024-12-23 | GSE284995 | GEO

Regulation of Liver Regeneration by Hepatocyte O-GlcNAcylation in Mice

Project description:We studied the role of the post-translational modification called O-GlcNAcylation during liver regeneration. Here we generated O-GlcNAc transferase (OGT-KO) and O-GlcNAcase (OGA-KO) hepatocyte-specific knock-out mice. 70% partial hepatectomy (PHX) was performed to induce liver regeneration. We showed that OGA-KO mice had normal liver regeneration whereas OGT-KO mice had a defect in the termination of liver regeneration.

2022-02-25 | GSE188882 | GEO

Mecp2 fine-tunes quiescence exit by targeting nuclear receptors [ChIP-Seq]

Project description:To identify the Mecp2-dependent transcriptome genome-wide during the very early stage of liver regeneration, we mapped the binding landscape of Mecp2 in control and MeCP2-KO livers before and after PHx using ChIP-seq. we mapped the binding landscape of Mecp2 in control livers before and after PHx by filtering out peaks identified in Mecp2-cKO livers. we identified a total of 14640 and 15350 Mecp2-binding genes before and after PHx in the Mecp2 control liver, respectively.

2024-04-26 | GSE227727 | GEO

HMGB2 is important for liver regeneration through transient accumulation of lipid droplets in hepatocytes

Project description:Liver regeneration is an well orchestrated compensatory process that regulated by multiple factors. We recently reported the importance of chromatin protein, a high-mobility group box 2 (HMGB2) in mouse liver regeneration, however, it’s molecular mechanism is not yet understood. In this study, we aimed to study how HMGB2 regulates hepatocyte proliferation during liver regeneration. Wild-type (WT) and HMGB2-knockout (KO) mice were 70% partial hepatectomized (PHx), and liver tissues were analyzed by microarray, immunohistochemistry, qPCR and western blotting. In vivo experimental findings were confirmed by in vitro experiments using HMGB2 gene knockdown in combination with de novo lipogenesis model. In WT mouse, HMGB2-positive hepatocytes were co-localized with cell proliferation markers, whereas, hepatocyte proliferation was significantly decreased in HMGB2-KO mice. Oil red-O staining detected the transient accumulation of lipid droplets at 12-24 h in WT mouse livers, however, decreased amount of lipid droplets were found in HMGB2-KO mouse livers, and it was prolonged until 36 h. Microarray, immunohistochemistry and qPCR results were demonstrated that lipid metabolism related genes were significantly decreased in HMGB2-KO mouse livers. In vitro experiments demonstrated that decreased lipid droplets in HMGB2-knockdown cells correlated with decreased cell proliferation activity. HMGB2 is involved in the regulation of liver regeneration through transient accumulation of lipid droplets in hepatocytes.

2023-10-14 | GSE244551 | GEO

Cooperative role of Lymphotoxin Beta Receptor and Tumor Necrosis Factor Receptor p55 in murine liver regeneration (PHx WT vs KO)

Project description:The liver exhibits a unique capacity for regeneration in response to injury. Lymphotoxin β Receptor (LTβR), a core member of the Tumor Necrosis Factor (TNF)/TNF Receptor (TNFR) superfamily is known to play an important role in this process. However, LTβR functions in the pathophysiological alterations and molecular mechanisms of liver regeneration are so far ill-characterized. Interestingly, LTβR / mice suffered from increased and prolonged liver tissue damage after 70 % hepatectomy (PHx), a finding accompanied by elevated alkaline phosphatase levels and deregulated bile acid (BA) homeostasis. Pronounced differences in the expression patterns of genes relevant for BA synthesis and recirculation were observed. Transcriptome analysis revealed a marked disparity in gene expression programs in LTβR / vs. WT liver tissue, where gene ontology (GO) terms related to transcription, gene expression and metabolic pathways were over-represented in the latter. In addition, murinoglobulin 2 (Mug2), a gene product to date not implicated in liver regeneration, was identified as one of the most differentially regulated genes after PHx in WT compared to LTβR / and TNFRp55-/- livers. LTβR and TNFRp55 share downstream signaling elements. TNFRp55 is known to also play an important role in liver regeneration after PHx. Therefore, LTβR / mice were treated with Etanercept to create mice functionally deficient in both signaling pathways. Strikingly, the combined blockade of TNFR and LTβR signaling leads to complete failure of liver regeneration resulting in death within 24 to 48 hours after PHx. LTβR is essential for efficient liver regeneration and cooperates with TNFRp55 in this process. Differences in survival kinetics strongly suggest distinct functions for these two cytokine receptors in liver regeneration. Failure of TNFR and LTβR signaling renders liver regeneration impossible.

2024-02-25 | GSE67263 | GEO

Cooperative role of Lymphotoxin β Receptor and Tumor Necrosis Factor Receptor p55 in murine liver regeneration (PHx Control vs Enbrel)

2024-02-25 | GSE74531 | GEO

RNA sequencing of undamaged, PHx liver and Hepatocyte organoids

Project description:To investigate the cellular and molecular mechanisms that initiate liver regeneration and liver organoid formation, we performed RNA sequencing in the following cell types: hepatocytes from undamaged livers of mice as well as 6 h, 12 h, 24 h, 48 h, 72 h, 7 d, 14 d, 21 d of liver regeneration after PHx. Hep-Orgs were isolated from adult male mice hepatocytes and cultured for passages.

2025-04-08 | GSE243302 | GEO

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