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Targeted deletion of mouse Slc25a28 (Mitoferrin2) reveals Mitoferrin1 and Mitoferrin2 are necessary for liver regeneration and cell proliferation

ABSTRACT: Targeted deletion of mouse Slc25a28 (Mitoferrin2) reveals Mitoferrin1 and Mitoferrin2 are necessary for liver regeneration and cell proliferation

PROVIDER: PRJNA602174 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10915485.fastq.gz	Fastqsanger.gz
	SRR10915486.fastq.gz	Fastqsanger.gz
	SRR10915487.fastq.gz	Fastqsanger.gz
	SRR10915488.fastq.gz	Fastqsanger.gz
	SRR10915489.fastq.gz	Fastqsanger.gz

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Bile acid flux is necessary for normal liver regeneration

Project description:Bile acid return from the intestine and attendant signaling is necessary for liver regeneration after partial hepatectomy or CCl4 injury Three groups of rat liver were examined at 4 time points (0, 4h, 12h, 24h) after partial hepatectomy; RNA from whole rat liver was isolated and deep sequencing was performed using the Illumina TruSeq platform

2014-02-05 | E-GEOD-54673 | biostudies-arrayexpress

Bile acid flux is necessary for normal liver regeneration

Project description:Bile acid return from the intestine and attendant signaling is necessary for liver regeneration after partial hepatectomy or CCl4 injury

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Targeted deletion of mouse Slc25a28 (Mitoferrin2) reveals Mitoferrin1 and Mitoferrin2 are necessary for liver regeneration and cell proliferation

Project description:Hepatocyte-specific loss of Slc25a37 (Mitoferrin1) in Mitoferrin2-/- mice did not affect animal viability or liver size suggesting that there must be alternative hepatocyte mitochondrial iron importers that function in the absence of Mitoferrins.

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Liver regeneration after cholestatic damage induced by Rbpj deletion

Project description:Liver regeneration after cholestatic damage induced by Rbpj deletion

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Liver regeneration after cholestatic damage induced by Rbpj deletion

Project description:Liver cholestasis is a chronic liver disease (CLD) which belongs to a major health problem. Cholestasis is characterised by a decrease in bile flow due to impaired secretion by hepatocytes or by obstruction of bile flow through intra- or extrahepatic bile ducts. Thereby cholestasis can induce ductal proliferation, hepatocyte injury and liver fibrosis. Notch signalling promotes the formation and maturation of ductular reactions. We investigated the liver regeneration process in the context of cholestasis induced by disruption of the Notch signalling pathway. Liver-specific deletion of Rbpj, which represents a key regulator of Notch signalling, induces severe cholestasis through impaired IHBD maturation, severe necrosis and increased lethality. Deregulation of the biliary compartment and cholestasis are associated with change of several signalling pathways including the Hippo pathway resulting in upregulation of SOX9, which is associated with transdifferentiation of hepatocytes. SOX9 upregulation in cholestatic liver injury in vitro is independent of Notch signalling. We could comprehensively address that Rbpj depletion is followed by deregulation of YAP/TEAD, which influences transdifferentiation of hepatocytes and thereby contributing to liver regeneration. In this study the liver regeneration process was analyzed in 4 weeks old Rbpj knockout mice and compared to 4 weeks old Rbpj wildtype mice.

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NADPH oxidase 4 (Nox4) deletion accelerates liver regeneration in mice

Project description:NADPH oxidase 4 (Nox4) deletion accelerates liver regeneration in mice

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Dynamic miRNA Expression Patterns During Retina Regeneration in Zebrafish: Loss of Dicer Inhibits Regeneration

Project description:Background: Adult zebrafish spontaneously regenerate their retinas after damage. Although a number of genes and signaling pathways involved in regeneration have been identified, the extent of mechanisms regulating regeneration is unclear. Small non-coding RNAs, microRNAs (miRNAs), that regulate regeneration of various tissues in lower vertebrates were examined for their potential roles in regulating zebrafish retinal regeneration. Results: To investigate the requirement of miRNAs during zebrafish retinal regeneration, we knocked down the expression of the miRNA-processing enzyme Dicer in retinas prior to light-induced damage. Dicer loss significantly reduced proliferation of Müller glia-derived neuronal progenitor cells during regeneration. To identify individual miRNAs with roles in retina regeneration, we collected retinas at different stages of light damage and performed small RNA high-throughput sequencing. We identified subsets of miRNAs that were differentially expressed during active regeneration but returned to basal levels once regeneration was completed. To validate the roles of differentially expressed miRNAs, we knocked down 6 different miRNAs that were upregulated in expression during regeneration and demonstrated that they have distinct effects on neuronal progenitor cell proliferation and migration during retina regeneration. Conclusions: miRNAs are necessary for retinal regeneration. miRNA expression is dynamic during regeneration. miRNAs function during initiation and progression of retinal regeneration. Identification of miRNAs before, during and after completion of zebrafish retinal regeneration

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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.

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Dynamic remodeling of translation programs drives hepatocyte proliferation during liver regeneration

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Tob1 is a Constitutively Expressed Repressor of Liver Regeneration

Project description:How proliferative and inhibitory cell signals integrate to control liver regeneration remains poorly understood. A screen for antiproliferative factors repressed after liver injury identified Tob1, a member of the PC3/BTG1 family of mitoinhibitory molecules as a target for further evaluation. Tob1 protein decreases after 2/3 hepatectomy in mice secondary to post-transcriptional mechanisms. Deletion of Tob1 increases hepatocyte proliferation and accelerates restoration of liver mass after hepatectomy. Down-regulation of Tob1 is required for normal liver regeneration and Tob1 controls hepatocyte proliferation in a dose-dependent fashion. Tob1 associates directly with both Caf1 and the Cyclin/cdk complex to modulate kinase activity. In addition, Tob1 has significant effects on the transcription of critical cell cycle components, including E2F targets and genes involved in p53 signaling. These studies provide direct evidence that levels of an inhibitory factor control the rate of liver regeneration. Our data identify Tob1 as a crucial check-point molecule that acts by by modulating levels and activity of cell cycle proteins. Samples from wild type and Tob1 null mice as normal adults and 24 hours after 2/3 hepatectomy are used. Each experimental point used data from two chips, each having a different set of three pooled animals. In summary we had 8 chips: 2 for WT time 0, 2 for WT time 24, 2 for KO time 0, 2 for KO time 24.

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