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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: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE159498 | GEO | 2020/10/14

REPOSITORIES: GEO

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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

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

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

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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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RNA-seq of cardiac-specific Cdk1 knockout mice at 4 days after experimental myocardial infarction

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 (CM) 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 CM regeneration or promotes maladaptive remodeling, leading to compromised cardiac function. Overview of the Experimental Workflow: We performed RNA-sequencing (RNA-seq) on heart tissue collected from both wild-type (WT) and cardiac-specific Cdk1 knockout mice subjected to experimental MI. Heart samples were collected 4 days to capture dynamic transcriptional changes associated with Cdk1 loss. Comparative transcriptomic analysis between WT and knockout samples will reveal differentially expressed genes and signaling pathways involved in cardiomyocyte proliferation, apoptosis, and fibrosis. These insights may uncover key pathways driving heart regeneration or degeneration in the absence of Cdk1.

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Regulation of S-phase transcription factors by Cdk1

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

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