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Effects of vitamin A on Ventricular myocardium gene expression [right ventricle]

ABSTRACT: LRAT knockout mice on vitamin A sufficient or deficient diets were compared to age-matched wild type mice on a vitamin A sufficient diet RNA was isolated from right ventricle of the heart and one array was run for each sample.

ORGANISM(S): Mus musculus

SUBMITTER: Douglas Sawyer

PROVIDER: E-GEOD-74905 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Effects of vitamin A deficiency in the postnatal mouse heart: role of hepatic retinoid stores.

Asson-Batres Mary Ann MA Ryzhov Sergey S Tikhomirov Oleg O Duarte Christine W CW Congdon Clare Bates CB Lessard Craig R CR McFarland Samuel S Rochette-Egly Cecile C Tran Truc-Linh TL Galindo Cristi L CL Favreau-Lessard Amanda J AJ Sawyer Douglas B DB

American journal of physiology. Heart and circulatory physiology 20160415 11

To determine whether hepatic depletion of vitamin A (VA) stores has an effect on the postnatal heart, studies were carried out with mice lacking liver retinyl ester stores fed either a VA-sufficient (LRVAS) or VA-deficient (LRVAD) diet (to deplete circulating retinol and extrahepatic stores of retinyl esters). There were no observable differences in the weights or gross morphology of hearts from LRVAS or LRVAD mice relative to sex-matched, age-matched, and genetically matched wild-type (WT) cont ...[more]

PMID: 27084391

Similar Datasets

Effects of vitamin A on ventricular myocardium gene expression [left ventricle]

Project description:LRAT knockout mice on vitamin A sufficient or deficient diets were compared to age and gender matched wildtype mice on a vitamin A sufficient diet RNA was isolated from the left ventricle of the heart and one array was run for each sample.

2016-07-25 | E-GEOD-74904 | biostudies-arrayexpress

Effects of vitamin A on ventricular myocardium gene expression

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-07-25 | E-GEOD-74906 | biostudies-arrayexpress

In Vivo Endothelial Cell Heterogeneity

Project description:Endothelial cells from nine steady state tissues and two regenerating tissues (bone marrow and liver) were intravitally labeld, isolated via flow sorting, and immediately processed for RNA extraction. When of sufficient quality, the RNA was amplified and hybridized. For comparison, Human Emybryonic Stem Cell-derived Endothelial cells (hESC-ECs) were differentiated and isolated based on similarities to the adult mouse counterparts. Endothelial cells were labeled via intravitally labeling of the vascular bed 8 minutes prior to sacrifice with minimally three markers to identify endothelial cells followed by flow sorting.

2013-07-15 | E-GEOD-47067 | biostudies-arrayexpress

Inflammatory profile of NOD.Batf3-/- islets

Project description:NOD mice deficient in the transcription factor Batf3 never develop diabetes. The goal of this study was to determine if NOD.Batf3-/- mice islets had any inflammatory signature associated with type 1 diabetes. Islets of Langerhans were isolated from NOD, NOD.Batf3-/-, and NOD.Rag1-/- and then compared to determine inflammatory gene profiles. At 6 and 8 weeks of age, NOD.Batf3-/- islets had an absence of inflammatory gene expression and were almost identical to uninflamed NOD.Rag1-/- islets. This work shows that absence of the Batf3 transcription factor is sufficient to prevent all the inflammatory sequelae of autoimmune diabetes. RNA was isolated from the pancreatic islets of Langerhans of 27 experimental mice. Mice were aged either 6 or 8 weeks. Three genotypes were tested: NOD, NOD.Rag1-/-, and NOD.Batf3-/-. There were 3-6 biological replicates per condition. All mice were female. All data was normalized using RMA in Arraystar.

2014-09-29 | E-GEOD-61847 | biostudies-arrayexpress

Genome-wide analysis revealed a crosstalk between p53 and the pluripotent gene networks in mouse embryonic stem cells (expression)

Project description:The tumor suppressor p53 regulates the differentiation of embryonic stem (ES) cells upon DNA damage. However, our understanding of this critical tumor suppressive role of p53 in ES cells is limited, mainly because of the lack of molecular mechanism. Here, we report a widespread cross-regulation of p53-mediated DNA damage signaling and the pluripotent gene network in ES cells using chromatin-immunoprecipitation assay-based sequencing (ChIP-seq) and gene expression microarray. Upon DNA damage, p53 directly regulates the transcription of 3644 genes (p<0.005) in mouse ES cells. Genome-wide analysis revealed a dramatic difference between the regulation of p53-activated and -repressed genes. p53 mainly regulates the promoter regions of activated genes, whereas the main regulatory regions for repressed genes reside in distal regions. Among p53-repressed genes, many are pluripotent transcription factors of ES cells, such as Oct4, Nanog, Sox2, Esrrb, c-Myc, n-Myc and Sall4. Strikingly, these transcriptional factors also directly regulate the transcription of the Trp53 gene, highlighting a previously under-estimated transcriptional regulation of p53 in ES cells. Therefore, p53 signaling and ES pluripotent transcriptional networks form an intertwined circuitry. Together, our results provide mechanistic insights into the crosstalk of p53-mediated DNA damage and ES cell "stemness" transcriptional gene networks and shed light on the tumor suppressive function of p53 in ES cells. The goal of this experiment is to identify the gene expression changes after adriamycin treatment in a p53-dependent manner. Total six samples: triplicates for untreated mES cells and triplicates for mES cells treated with adriamycin.

2012-03-05 | E-GEOD-26360 | biostudies-arrayexpress

Expression data of liver samples of dex or vehicle treated wildtype and HDAC6- knockout C57Bl/6 mice respectively

Project description:In the present study, we investigated the importance of histone deacetylase 6 (HDAC6) for glucocorticoid receptor (GR) mediated effects on glucose metabolism, and its potential as a therapeutic target for the prevention of glucocorticoid (GC)-induced diabetes. Dexamethasone (dex)-induced hepatic glucose output and GR translocation were analysed in wildtype (wt) and HDAC6-deficient (HDAC6ko) mice. The effect of the specific HDAC6-inhibitor tubacin was analysed in-vitro. Wt and HDAC6ko mice were subjected to 3 weeks dex treatment before analysis of glucose and insulin tolerance. HDAC6ko mice showed impaired dex-induced hepatic GR translocation. Accordingly, dex induced expression of a large number of hepatic genes was significantly attenuated in mice lacking HDAC6 and by tubacin in-vitro. Glucose output of primary hepatocytes from HDAC6ko mice was diminished. A significant improvement of dex-induced whole-body glucose intolerance as well as insulin resistance in HDAC6ko mice compared to wt littermates was observed. The present study demonstrates that HDAC6 is an essential regulator of hepatic GC stimulated gluconeogenesis and impairment of whole body glucose metabolism through modification of GR nuclear translocation. Selective pharmacological inhibition of HDAC6 may provide a future therapeutic option against the pro-diabetogenic actions of GCs. In this dataset, we include the expression data obtained from isolated RNA of dissected mouse livers using wildtype and HDAC6 deficient animals which were treated over a timespan of 3 weeks with 1mg/kg dexamethasone and vehicle respectively. These data are used to show the hdac6-deficiency mediated attenuation of several dexamethasone induced genes. 12 samples in total were analyzed. 3 samples of different animals of each group (wt vehicle, wt dexamethasone, hdac6ko vehicle and hdac6ko dexamethasone)

2011-12-07 | E-GEOD-34229 | biostudies-arrayexpress

Expression data from Tcf1-expressing Thy1+CD25+ T lineage cells

Project description:We used microarrays to perform a global gene expression analysis in Tcf1-expressing Thy1+CD25+ T lineage cells that develop on OP9 stroma in the absence of Notch1 signals. We compare this to the starting population, LMPP progenitors, and to control expressing T lineage cells that developed on OP9 stroma expressing Notch ligand DL4. The overall goal of this study was to determine if Tcf1 initiates T lineage specification in lymphoid progenitors. We found that Tcf1 was sufficient to upregulate many T lineage genes as compared to control expressing progenitors on OP9-DL4. Abstract of manuscript: The thymus imposes the T cell fate on incoming multipotent progenitors, but the molecular mechanisms are poorly understood. We show that transcription factor Tcf1 initiates T-lineage-specific gene expression. Tcf1 is downstream of Notch1 signaling and expressed in early T-cell progenitors. Progenitors deficient for Tcf1 are unable to initiate normal T-lineage specification. Conversely, ectopic expression of Tcf1 in hematopoietic progenitors is sufficient to induce expression of T-lineage specific genes in vitro. Thus, our study identifies Tcf1 as critically involved in the establishment T cell identity. Wiltype LMPPs were isolated by a FACSAria cell sorter and retrovirally transduced with a Tcf1-containing (Tcf1-VEX) or control vector (VEX) retrovirus. Tcf1-expressing cells and control-vector expressing cells were then seeded on OP9 stroma or OP9 stroma expressing Notch ligand DL4, respectively. On day 10, Thy1+CD25+ T lineage cells were sorted from Tcf1-expressing cells on OP9 stroma and compared to sorted LMPPs and Thy1+CD25+ T lineage cells that developed from control-vector expressing cells on OP9-DL4.

2011-08-03 | E-GEOD-26560 | biostudies-arrayexpress

The effect of Crem absence on gene expression in mouse liver.

Project description:CREM (cAMP responsive element modulator) together with CREB and ATF-1 belong to the CREB family of transcriptional factors, that respond to cyclic AMP signaling and bind to cAMP responsive element (CRE) sites in promoters of selected genes. CREM can produce isoforms that have either activating or repressing functions, depending on the transcription of specific exons. In this dataset, we include the expression data obtained from wild-type (WT) and Crem knock-out (KO) mouse liver. Several comparisons were made. KO<WT at 0h, KO<WT at 12 h, 0h<12h in WT and 0h<12h in KO. 4 condition experiment: 2 strains (WT, Crem-/-), 2 time points (0h and 12h). 5 biological replications per condition.

2014-05-25 | E-GEOD-29594 | biostudies-arrayexpress

Whole-genome study reveals distinct mechanisms used by p53 to regulate activated and repressed genes in embryonic stem cells

Project description:This SuperSeries is composed of the following subset Series: GSE26360: Genome-wide analysis revealed a crosstalk between p53 and the pluripotent gene networks in mouse embryonic stem cells (expression) GSE26361: Genome-wide analysis revealed a crosstalk between p53 and the pluripotent gene networks in mouse embryonic stem cells (ChIP-Seq) Refer to individual Series

2012-03-05 | E-GEOD-26362 | biostudies-arrayexpress

Effect of dietary fat and cholesterol on hepatic gene expression of liver-specific Cyp51 knockout male and female mice

Project description:Cholesterol is one of the key molecules in mammals and the most striking examples of its deficiency are the inborn errors of cholesterol biosynthesis that manifest in severe whole body phenotypes. Liver, the principal site of cholesterol homeostasis, has rarely been investigated in these defects. We thus focused on the hepatocyte-specific deletion of lanosterol 14α-demethylase (CYP51) catalyzing the rate-limiting step in the post-squalene part of cholesterol synthesis. Liver-specific Cyp51 KO (LKO or K) and littermate control (LWT or W) mice (129/Pas (10%) × C57BL/6J (90%)) of both sexes (F and M) were investigated in the context of different nutritional availability of fat and cholesterol (standard laboratory diet without cholesterol (LFnC or L), high-fat diet without cholesterol (HFnC or H) and high-fat diet with cholesterol (HFC or C) due to the known sexual dimorphism in hepatic gene expression, where lipid metabolic pathways are among the most biased. 3 condition experimental design: 3 diets (LFnC or L, HFnC or H, HFC or C), 2 genotypes (LWT or W, LKO or K), 2 sexes (F, M), 3 biological replicates per condition, 36 mice altogether

2015-05-28 | E-GEOD-58271 | biostudies-arrayexpress

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