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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse Serum response factor (Srf) conditional knockout in the mouse liver

ABSTRACT: Serum response factor (SRF) is a transcription factor that binds to the serum response element (SRE) of genes that are expressed in response to mitogens. SRF plays essential roles in muscle and nervous system development; however, little is known about the role of SRF during liver growth and function. To examine the function of SRF in the liver, we generated mice in which the Srf gene was specifically disrupted in hepatocytes. The survival of mice lacking hepatic SRF activity was lower than that of control mice; moreover, surviving mutant mice were smaller and had lower blood glucose and triglyceride levels compared with control mice. Srf-deficient livers were also smaller than control livers, hepatocyte morphology was abnormal, and liver-cell proliferation and viability was compromised. Gene array and quantitative RT-PCR analysis of SRF depleted livers revealed a reduction in mRNAs encoding components of the growth hormone/IGF1 pathway, cyclins, several metabolic regulators, and cytochrome p450 enzymes. Conclusion: SRF is essential for hepatocyte proliferation and survival, liver function, and control of postnatal body growth by regulating hepatocyte gene expression. Experiment Overall Design: Total RNA was harvested from the following sources and used for Affymetrix array analysis following manufacturer defined protocols: Experiment Overall Design: control liver (Srf loxP/+ AlfpCre): 3 male mice (3 weeks old) Experiment Overall Design: mutant liver (Srf loxP/loxP AlfpCre): 3 male mice (3 weeks old), tissue used lacked Srf

ORGANISM(S): Mus musculus

SUBMITTER: Stephen Duncan

PROVIDER: E-GEOD-13333 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Srf conditional knockout in the mouse liver

Project description:Serum response factor (SRF) is a transcription factor that binds to the serum response element (SRE) of genes that are expressed in response to mitogens. SRF plays essential roles in muscle and nervous system development; however, little is known about the role of SRF during liver growth and function. To examine the function of SRF in the liver, we generated mice in which the Srf gene was specifically disrupted in hepatocytes. The survival of mice lacking hepatic SRF activity was lower than that of control mice; moreover, surviving mutant mice were smaller and had lower blood glucose and triglyceride levels compared with control mice. Srf-deficient livers were also smaller than control livers, hepatocyte morphology was abnormal, and liver-cell proliferation and viability was compromised. Gene array and quantitative RT-PCR analysis of SRF depleted livers revealed a reduction in mRNAs encoding components of the growth hormone/IGF1 pathway, cyclins, several metabolic regulators, and cytochrome p450 enzymes. Conclusion: SRF is essential for hepatocyte proliferation and survival, liver function, and control of postnatal body growth by regulating hepatocyte gene expression.

2009-03-01 | GSE13333 | GEO

LKB1 and Notch deletion in mouse liver

Project description:We characterize the phenotype of mice in which the deletion of Lkb1 has been targeted in the liver. Lack of Lkb1 in the liver results in bile duct paucity leading to cholestasis. This phenotype is similar to that obtained upon inactivation of Notch signaling in the liver. We test the hypothesis of a functional overlap between the Lkb1 and Notch pathways by gene expression profiling of livers deficent in Lkb1 or in the Notch mediator RbpJκ. We used AlfpCre mice for liver-specific deletion of LKB1 that were crossed with a conditional knockout mouse model (LKB1 floxed mice). We used also AlfpCre mice for liver-specific inactivation of the Notch pathway. AlfpCre mice were crossed with the RbpJκ floxed mice. RNA was extracted from the liver of LKB1 KO mice (Lkb1Floxed, AlfpCre positive mice) and their wild-type counterpart (Lkb1Floxed, AlfpCre negative mice). RNA was also extracted from liver of RbpJK KO mice (RbpJK floxed, AlfpCre positive) and their wild type mice (RbpJK floxed, AlfpCe negative).

2015-12-08 | GSE75564 | GEO

LKB1 and Notch deletion in mouse liver

Project description:We characterize the phenotype of mice in which the deletion of Lkb1 has been targeted in the liver. Lack of Lkb1 in the liver results in bile duct paucity leading to cholestasis. This phenotype is similar to that obtained upon inactivation of Notch signaling in the liver. We test the hypothesis of a functional overlap between the Lkb1 and Notch pathways by gene expression profiling of livers deficent in Lkb1 or in the Notch mediator RbpJÎº. We used AlfpCre mice for liver-specific deletion of LKB1 that were crossed with a conditional knockout mouse model (LKB1 floxed mice). We used also AlfpCre mice for liver-specific inactivation of the Notch pathway. AlfpCre mice were crossed with the RbpJÎº floxed mice. RNA was extracted from the liver of LKB1 KO mice (Lkb1Floxed, AlfpCre positive mice) and their wild-type counterpart (Lkb1Floxed, AlfpCre negative mice). RNA was also extracted from liver of RbpJK KO mice (RbpJK floxed, AlfpCre positive) and their wild type mice (RbpJK floxed, AlfpCe negative). 6 samples for the liver-specific deletion of LKB1 corresponding to 3 KO LKB1 (Cre positive) and 3 normal liver (Cre negative). 6 samples for the liver-specific inactivation of the Notch pathway corresponding to 3 KO RbpJk (Cre positive) and 3 normal liver (Cre negative).

2015-12-08 | E-GEOD-75564 | biostudies-arrayexpress

Comprehensive proteomic and transcriptomic characterization of hepatic expression signatures affected in p14 liver conditional knockout mice

Project description:Scaffold proteins regulate intracellular MAP kinase signaling by providing critical spatial and temporal specificity. We have shown previously that the scaffold protein MEK1 partner (MP1) is localized to late endosomes by the adaptor protein p14. Using conditional gene disruption of p14 in livers of mice we analysed protein and transcript signatures in tissue samples. Further biological network analysis predicted that the differentially expressed transcripts and proteins are involved in cell cycle progression and regulation of cellular proliferation. Although some of the here identified signatures were previously linked to phospho-ERK activity, most of them were novel targets of late endosomal p14/MP1/MEK/ERK signaling module. Finally, the proliferation defect was confirmed in a chemically induced liver regeneration model in p14 liver knock-out mice. Conditional liver p14 KO mice were generated by mating p14 f/f mice with mice expressing Cre recombinase under control of Alb promoter and alpha-fetoprotein enhancer. The obtained p14 floxed/floxed;AlfpCre(p14 liver KO) mice were used in experiments as KO mice. To prevent the influence of AlfpCre transgene we used p14 +/+;AlfpCre mice as a control. All mice were derived in a C57BL/6 background and were six weeks old.

2011-02-01 | GSE24461 | GEO

Liver tissue from liver specific Vps33b knockout (Vps33bfl/fl-AlfpCre) and control (Vps33bfl/fl) mice

Project description:Liver tissue from Vps33b liver ko (Vps33bfl/fl-AlfpCre) mice is a model of liver disease associated with ARC syndrome, an autosomal recessive inherited metabolic disorder cause by mutations in VPS33B or VIPAS39. ARC is a multisystem disorder, with liver and kidneys affected in particular. Defects in hepatocyte polarity have been identified. Affymetrix arrays were used to characterise the changes in the liver transcriptome when Vps33b is not expressed. Mouse liver tissue, 10 samples in total, 4 from control mice, 6 from ko mice.

2016-06-10 | E-GEOD-83192 | biostudies-arrayexpress

Expression data from mouse liver

Project description:LASS2 is expressed mostly in human liver. We explored roles of LASS2 in pathogenesis of hepatic steatosis. Hepatocyte-specific LASS2 knockout (LASS2-/-) mice were generated using Cre-LoxP system. LASS2-/- and wild-type (WT) mice were fed with chow or high-fat diet (HFD). We performed global gene expression analysis for the mice livers in accordance with standard Affymetrix protocols to explore signaling pathways involved by LASS2 deficiency.

2016-12-27 | GSE92912 | GEO

High Mobility Group Box Protein 1 is Dispensable for Autophagy and Mitochondrial Quality Control in Vivo

Project description:Gene expression of livers with hepatocyte-specific deletion of Hmgb1 was compared to control livers with floxed Hmgb1 Hmgb1-deleted livers (from mice expressing Albumin-Cre and floxed Hmgb1) and control liver (mice expressing only floxed Hmgb1) Whole liver from 8 week old mice was used. Both groups are littermates, and have been backcrossed to C57Bl/6 five times.

2016-04-11 | GSE49824 | GEO

Cyldko

Project description:Effect of Cyld inactivation in liver. The Cyld gene was conditionally inactivated specifically in the liver by crossing mice carrying floxed exon 9 allele of Cyld with Alfp-Cre transgenic mice. Liver RNAs from Cyld lox/lox-AlfpCre mice were compared with RNAs prepared from the livers of wild type littermates.

2012-02-01 | E-MEXP-3478 | biostudies-arrayexpress

Chromatin immunoprecipitation of wild type and Foxa2 knock-out mouse liver using anti-HNF6 anitbodies to test whether Foxa2 inhibits HNF6-mediated transcription in the liver

Project description:The aim of this study was to test, in vivo, if Foxa2 inhibits HNF6-mediated transcription in the liver. We utilized hepatocyte-specific gene ablation of Foxa2 and the Mouse PromoterChip BCBC 3.0 and Mouse PancChip 5.0 cDNA microarrays to investigate HNF6 binding to its target promoters in vivo in the presence or absence of Foxa2. For the mouse promoter microarray analysis, chromatin immunoprecipitation using anti-HNF6 antibodies was performed on chromatin isolated from Foxa2loxP/loxP Alfp.Cre and control mouse livers. Along with sheared genomic DNA (common reference), the immunoprecipitated DNA was amplified, labeled and hybridized to the Mouse PromoterChip BCBC 3.0. For microarray analysis of gene expression, liver RNAs were isolated from three Foxa2loxP/loxP Alfp.Cre and three control mice. RNAs were reverse transcribed, labeled, and hybridized to the Mouse PancChip 5.0. Overall, our studies demonstrate that HNF6 binds to and regulates its target promoters in vivo in the presence and absence of Foxa2 and that the expression levels of HNF6 targets are not influenced by Foxa2.

2007-09-14 | E-CBIL-36 | biostudies-arrayexpress

Comprehensive proteomic and transcriptomic characterization of hepatic expression signatures affected in p14 liver conditional knockout mice

2011-02-01 | E-GEOD-24461 | biostudies-arrayexpress

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