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Remodelling of whole-body lipid metabolism and a diabetic-like phenotype caused by loss of hepatic CDK1 and hepatocyte division

ABSTRACT: Remodelling of whole-body lipid metabolism and a diabetic-like phenotype caused by loss of hepatic CDK1 and hepatocyte division

PROVIDER: PRJNA669059 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12820608.fastq.gz	Fastqsanger.gz
	SRR12820609.fastq.gz	Fastqsanger.gz
	SRR12820610.fastq.gz	Fastqsanger.gz
	SRR12820611.fastq.gz	Fastqsanger.gz
	SRR12820612.fastq.gz	Fastqsanger.gz

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Remodelling of whole-body lipid metabolism and a diabetic-like phenotype caused by loss of hepatic CDK1 and hepatocyte division

Project description:Purpose was to identify transcriptomic changes in whole liver and isolated hepatocytes from 12 month old wild type and Cdk1 liver-specific knock-out (Cdk1 Liv-/-) mice.

2020-10-14 | GSE159498 | GEO

Remodeling of whole-body lipid metabolism and a diabetic-like phenotype caused by loss of CDK1 and hepatocyte division.

Project description:Cell cycle progression and lipid metabolism are well-coordinated processes required for proper cell proliferation. In liver diseases that arise from dysregulated lipid metabolism, proliferation is diminished. To study the outcome of CDK1 loss and blocked hepatocyte proliferation on lipid metabolism and the consequent impact on whole-body physiology, we performed lipidomics, metabolomics, and RNA-seq analyses on a mouse model. We observed reduced triacylglycerides in liver of young mice, caused by oxidative stress that activated FOXO1 to promote expression of Pnpla2/ATGL. Additionally, we discovered that hepatocytes displayed malfunctioning β-oxidation, reflected by increased acylcarnitines (ACs) and reduced β-hydroxybutyrate. This led to elevated plasma free fatty acids (FFAs), which were transported to the adipose tissue for storage and triggered greater insulin secretion. Upon aging, chronic hyperinsulinemia resulted in insulin resistance and hepatic steatosis through activation of LXR. Here, we demonstrate that loss of hepatocyte proliferation is not only an outcome but also possibly a causative factor for liver pathology.

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Loss of hepatocyte cell division leads to liver inflammation and fibrosis

Project description:Purpose was to identify transcriptomic changes in whole liver and isolated hepatocytes from 2 week old wild type and Cdk1 liver-specific knock-out (Cdk1 Liv-/-) mice.

2020-10-14 | GSE159497 | GEO

Wnt Signaling Regulates Hepatocyte Cell Division by a Transcriptional Repressor Cascade

Project description:Cell proliferation is tightly controlled by inhibitors that block cell cycle progression until growth signals relieve this inhibition, allowing cells to divide. In several tissues including the liver, cell proliferation is inhibited at mitosis by the transcriptional repressors E2F7 and E2F8, leading to formation of polyploid cells. Whether growth factors promote mitosis and cell cycle progression by relieving the E2F7/E2F8-mediated inhibition is unknown. We report here on a new mechanism of cell division control in the postnatal liver, in which Wnt/βcatenin signaling maintains active hepatocyte cell division through Tbx3, a Wnt target gene. Tbx3 directly represses transcription of E2F7 and E2F8, thereby promoting mitosis. This cascade of sequential transcriptional repressors, initiated by Wnt signals, provides a new paradigm for exploring how commonly active developmental signals impact cell cycle completion.

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Loss of hepatocyte cell division leads to liver inflammation and fibrosis

Project description:Loss of hepatocyte cell division leads to liver inflammation and fibrosis

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Wnt Signaling Regulates Hepatocyte Cell Division by a Transcriptional Repressor Cascade

Project description:Wnt Signaling Regulates Hepatocyte Cell Division by a Transcriptional Repressor Cascade

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INO80 Chromatin Remodelling Coordinates Metabolic Homeostasis with Cell Division

Project description:We performed RNA-seq across the yeast metabolic cycle (YMC) in wild-type and a strain lacking ARP5, a central component of the INO80 chromatin remodelling complex. We also perform ATAC-seq on the same samples to examine chromatin architecture across the YMC.

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Effect of Cell cycle regulator CDK1 on Cell Differentiation (RNA-IP CDK1 inh KD)

Project description:We addressed the role of cell cycle regulator CDK1 during differentiation by either inhibiting its activity with the specific inhibitor RO3306 (10µM) or by knocking its expression down using specific shRNAs, during mesendoderm differentiation. Human pluripotent stem cells (H9 cells) were synchronized in their cell cycle and then induced to differentiate into mesendoderm for 24h. shRNAs against CDK1 were induced 4 days before starting the differentiation. The CDK1 inhibitor was added to the medium 8h after the induction of differentiation. At the end of the experiment, the cells were harvested and processed for total RNA extraction. RNA-IP was carried out using RiboCluster Profiler RIP-Assay Kit (MBL) following the manufacture’s recommendations.

2021-05-31 | GSE130827 | GEO

Cdk1 controls global epigenetic landscape in embryonic stem cells

Project description:In this study, we found that in ES cells the majority of Cdk1 substrates are localized on chromatin. Cdk1 phosphorylates a large number of proteins involved in epigenetic regulation, including writers and erasers of all major histone marks. High levels of Cdk1 in ES cells phosphorylate and partially inactivate Dot1l, the histone H3 lysine 79 methyltransferase responsible for placing activating H3K79 marks on gene bodies. Decrease of Cdk1 activity during ES cell differentiation de-represses Dot1l, thereby allowing coordinated expression of differentiation genes. These analyses indicate that Cdk1 functions to maintain the epigenetic identity of ES cells.

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Project description:Biological Relevance and Intent of the Experiment: The objective of this study is to elucidate the role of Cdk1 in cardiac function, specifically its contribution to cardiomyocyte proliferation and response to injury. Using a heart-specific Cdk1 knockout mouse model, we investigate the molecular and cellular impact of Cdk1 deficiency in the context of myocardial infarction (MI). Cdk1 is known for its regulatory functions in cell cycle progression, and its absence may significantly affect cardiac repair mechanisms post-MI. This research aims to explore whether the lack of Cdk1 impairs cardiomyocyte regeneration or promotes maladaptive remodeling, leading to compromised cardiac function.

2024-12-02 | E-MTAB-14508 | biostudies-arrayexpress

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