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Expansion of hepatic tumor progenito cell population in PTEN deficient mice requires liver injury and is reversed by deletion of Akt2

ABSTRACT: We found that hepatic injury induced by PTEN loss establishes a selection pressure for tumorinitiating cells (TICs) to proliferate and form mixed lineage tumors. The Pten null mice demonstrate escalating levels of hepatic injury prior to proliferation of hepatic progenitors. Attenuation of hepatic injury by deleting Akt2 reduces progenitor cell proliferation and delays tumor development. Treatment of double mutant mice with 3,5-dietoxycarbonyl-1,4 dihydrocollidine (DDC) shows that the primary effect of AKT2 loss is attenuation of hepatic injury and not inhibition of progenitor cell proliferation in response to injury.

ORGANISM(S): Mus musculus

PROVIDER: GSE70501 | GEO | 2016/03/31

SECONDARY ACCESSION(S): PRJNA288881

REPOSITORIES: GEO

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Expansion of hepatic tumor progenito cell population in PTEN deficient mice requires liver injury and is reversed by deletion of Akt2

Project description:We found that hepatic injury induced by PTEN loss establishes a selection pressure for tumorinitiating cells (TICs) to proliferate and form mixed lineage tumors. The Pten null mice demonstrate escalating levels of hepatic injury prior to proliferation of hepatic progenitors. Attenuation of hepatic injury by deleting Akt2 reduces progenitor cell proliferation and delays tumor development. Treatment of double mutant mice with 3,5-dietoxycarbonyl-1,4 dihydrocollidine (DDC) shows that the primary effect of AKT2 loss is attenuation of hepatic injury and not inhibition of progenitor cell proliferation in response to injury. Pten/Akt2 double mutant (PtenloxP/loxP; Akt2-/-; Alb-Cre+) (Dm) were generated by crossing the PtenloxP/loxP; Alb-Cre+ (Pm) with the Akt2-/- mice [19]. Control animals are PtenloxP/loxP; Albumin (Alb)-Cre-.

2016-03-31 | E-GEOD-70501 | biostudies-arrayexpress

Deletion of Pten leads to liver steatosis and tumor formation

Project description:We found that deleting Pten in Albumin expressing cells results in liver steatosis as early as 1 month of age. The mice develop hyperplasia and tumor phenotypes starting at 7-8 months of age. At 12 months and beyond, all mice develope spontanous liver tumors of mixed lineage phenotypes dihydrocollidine (DDC) shows that the primary effect of AKT2 loss is attenuation of hepatic injury and not inhibition of progenitor cell proliferation in response to injury. Pten is deleted specifically in the liver (Pten loxP/loxP; Alb-Cre+). Liver tissues were analyzed at 3 months (steatosis stage) and 15 months (tumor stage)

2015-12-31 | E-GEOD-70681 | biostudies-arrayexpress

Deletion of Pten leads to liver steatosis and tumor formation

2015-12-31 | GSE70681 | GEO

Akt2 partners L6 myoblasts - Novel Endogenous, Insulin-Stimulated Akt2 Protein Interaction Partners in L6 Myoblasts

Project description:Insulin resistance and Type 2 diabetes are marked by an aberrant response in the insulin signaling network. The phosphoinositide-dependent serine/threonine kinase, Akt2, plays a key role in insulin signaling and glucose uptake, most notably within skeletal muscle. Protein-protein interaction regulates the functional consequence of Akt2 and in turn, Akt2’s role in glucose uptake. However, only few insulin-responsive Akt2 interaction partners have been identified in skeletal muscle cells. In the present work, rat L6 myoblasts, a widely used insulin sensitive skeletal muscle cell line, were used to examine endogenous, insulin-stimulated Akt2 protein interaction partners. Akt2 co-immunoprecipitation was coupled with 1D-SDS-PAGE and fractions were analyzed by HPLC-ESI-MS/MS to reveal Akt2 protein-protein interactions. The pull-down assay displayed specificity for the Akt2 isoform; Akt1 and Akt3 unique peptides were not detected. A total of 330 proteins were significantly enriched as bonafide Akt2 protein interaction partners. Among them, 226 were novel for any cell types. Furthermore, 59 were detected with a significantly increased (57) or decreased (2) association with Akt2 following insulin administration (n=4; p<0.05). Multiple pathways were identified for the novel Akt2 interaction partners, such as the EIF2 and ubiquitination pathways. These data suggest that multiple new endogenous proteins may associate with Akt2 under basal as well as insulin-stimulated conditions, providing further insight into the insulin signaling network.

2015-09-30 | PXD002557 | Pride

Effect of cardiomyocyte specific KO of AKT1, AKT2, and AKT1 + AKT2 on gene expression profile of the heart

Project description:In the mammalian heart AKT1 and AKT2 are the isoforms of the protein kinase AKT (protein kinase B) which are predominantly expressed. AKT isoforms exert common and specific functions in the field of metabolism, cellular growth, apoptosis and cell migration. To identify specific and common functions of AKT1 and AKT2 isoforms, we generated tamoxifen-inducible, cardiomyocyte-specific AKT1, AKT2, and AKT1+AKT2 double knockout mice (iCMAKT – KO mice). Inactivation of AKT isoforms was achieved by application of 4-OH-tamoxifen, which activates an OH-Tx inducible cre-recombinase expressed under the control of the αMHC-promoter (αMHC-mercremer). Transgenic mice expressing only the αMHCmercremer construct were also treated with OH-Tx and served as controls. To identify alterations in cardiac gene expression due to AKT deletion we analyzed gene expression profiles of control hearts, iCMAKT1, iCMAKT2 and iCMAKT1+2 hearts.

2017-11-30 | GSE86231 | GEO

Myocardial expression data from wild-type and akt2-/- mice

Project description:Wild-type (WT) C57Bl/6 and akt2-/- male mice. Keywords: RNA Expression Array Left ventricles (LV) from 12-16 week-old male wild type mice and age-matched akt2-/- mice

2010-11-19 | E-GEOD-19079 | biostudies-arrayexpress

Myocardial expression data from wild-type and akt2-/- mice

Project description:Wild-type (WT) C57Bl/6 and akt2-/- male mice. Keywords: RNA Expression Array

2010-11-19 | GSE19079 | GEO

RNA-seq data from livers of 6 month old Akt1F/F;Akt2-/- versus Akt1F/F;Akt2-/-;Alb-Cre mice

Project description:Finding diffrential gene expression gene expression in the livers of male mice after the deletion of Akt1 in th eliver of Akt2-/- mice.

2016-04-30 | GSE77862 | GEO

Prospective isolation of a bipotential clonogenic liver progenitor cell in adult mice

Project description:The molecular identification of adult hepatic stem/progenitor cells has been hampered by the lack of truly specific markers. To isolate putative adult liver progenitor cells, we used cell surface-marking antibodies, including MIC1-1C3, to isolate subpopulations of liver cells from normal adult mice or those undergoing an oval cell response and tested their capacity to form bilineage colonies in vitro. Robust clonogenic activity was found to be restricted to a subset of biliary duct cells antigenically defined as CD45–/CD11b–/CD31–/MIC1-1C3+/CD133+/CD26–, at a frequency of one of 34 or one of 25 in normal or oval cell injury livers, respectively. Gene expression analyses revealed that Sox9 was expressed exclusively in this subpopulation of normal liver cells and was highly enriched relative to other cell fractions in injured livers. In vivo lineage tracing using Sox9creERT2-R26RYFP mice revealed that the cells that proliferate during progenitor-driven liver regeneration are progeny of Sox9-expressing precursors. A comprehensive array-based comparison of gene expression in progenitor-enriched and progenitor-depleted cells from both normal and DDC (3,5-diethoxycarbonyl-1,4-dihydrocollidine or diethyl1,4-dihydro-2,4,6-trimethyl- 3,5-pyridinedicarboxylate)-treated livers revealed new potential regulators of liver progenitors.

2011-05-07 | GSE29121 | GEO

Gene expression analysis of Akt2 deficient murine naive CD4 T cells cultured in Th17-polarizing conditions for 36 hours

Project description:Akt1 and Akt2, isoforms of the serine threonine kinase Akt, are essential for T cell development. However, their role in peripheral T cell differentiation remains undefined. Using mice with germline deletions of either Akt1 or Akt2, we found that both isoforms are important for Th17 differentiation, although Akt2 loss had a greater impact than Akt1. To better understand the consequences of Akt2 deficiency in the setting of in vitro Th17 differentiation, we used microarray analysis to compare the transcriptional landscape of Akt2â/â and WT cells that had been cultured in Th17 polarizing conditions for 36 hours.

2016-07-03 | E-MTAB-4062 | biostudies-arrayexpress

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