E-MTAB-5441
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-5441 | ExpressionAtlas | 2017-02-09
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:CDK7 adipose tissue specific knockout mice
| PRJNA627425 | ENA
Project description:Mice without cardiac Bmal1 function develop severe progressive heart failure with age. To examine the mechanism underlying the failing heart phenotype observed in heart-specific Bmal1 knockout mice, microarray analyses were performed. The analyses revealed that broad classes of genes regulating cellular energy metabolism were upregulated or downregulated in the heart tissues of heart-specific Bmal1 knockout mice compared with those of control animals. Heart total RNA extracted from six animals per genotype (control and heart-specific Bmal1 knockout) was pooled and then used for a microarray analysis.
2014-09-27 | E-GEOD-61787 | biostudies-arrayexpress
Project description:Fibrosis is defined as an abnormal matrix remodeling and loss of tissue homeostasis due to excessive synthesis and accumulation of extracellular matrix proteins in tissues. At present, there is no effective therapy for organ fibrosis. Previous studies demonstrated that aged plasminogen activator inhibitor-1(PAI-1) knockout mice develop spontaneously cardiac-selective fibrosis without affecting any other organs including kidney. Therefore, the PAI-1 knockout model of cardiac fibrosis provides an excellent opportunity to find the igniter(s) of cardiac fibrosis and its status in unaffected organs. We hypothesized that differential expressions of profibrotic and antifibrotic genes in PAI-1 knockout hearts and unaffected organs lead to cardiac selective fibrosis. In order to address this prediction, we have used a genome-wide gene expression profiling of transcripts derived from aged PAI-1 knockout hearts and kidneys. The variations of global gene expression profiling were compared within four groups: wildtype heart vs. knockout heart; wildtype kidney vs. knockout kidney; knockout heart vs. knockout kidney and wildtype heart vs. wildtype kidney. Analysis of illumina-based microarray data revealed that several genes involved in different biological processes such as immune system processing, response to stress, cytokine signaling, cell proliferation, adhesion, migration, matrix organization and transcriptional regulation were affected in hearts and kidneys by the absence of PAI-1, a potent inhibitor of urokinase- and tissue-type plasminogen activator. Importantly, the expressions of a number of genes, involved in profibrotic pathways were upregulated or downregulated in PAI-1 knockout hearts compared to wildtype hearts and PAI-1 knockout kidneys. To our knowledge, this is the first comprehensive report on the influence of PAI-1 on global gene expression profiling in the heart and kidney and its implication in several biological processes including fibrogenesis. Total RNA was extracted from hearts and kidneys derived from three PAI-1 knockout (12- month old) and three wild-type mice (12-month old) using RNeasy Fibrous Tissue Mini Kit (Qiagen, Valencia, CA) following the manufacturer’s instructions. The quality of RNA (RNA Integrity, RIN) in all 12 samples (3 wildtype hearts; 3 PAI-1 KO hearts; 3 wildtype kidneys; and 3 PAI-1 KO kidneys) was checked using the bioanalyzer. We have used a genome-wide gene expression profiling of transcripts derived from aged PAI-1 knockout hearts and kidneys. The variations of global gene expression profiling were compared within four groups: wildtype heart vs. knockout heart; wildtype kidney vs. knockout kidney; knockout heart vs. knockout kidney and wildtype heart vs. wildtype kidney.
2014-04-23 | E-GEOD-46320 | biostudies-arrayexpress
Project description:Genome-wide transcriptome analyses of transgenic mice, that express Cre recombinase flanked by mutated estrogen receptors (MerCreMer; mcm), and carry loxP-flanked sequences of p53 and Mdm2 was performed in the presence and absence of Tamoxifen.<br>The molecular mechanisms underlying heart failure remain poorly understood. As such, identifying the factors which effectively maintain cardiac tissue homeostasis is of great scientific and clinical importances. The tumor suppressor Trp53 (p53) inhibits cell growth after acute stress by regulating gene transcription. The mammalian genome contains hundreds of p53 binding sites. However, whether p53 participates in the regulation of cardiac tissue homeostasis under normal conditions is not known. To examine the physiologic consequences of p53 and Mdm2 ablation in adult cardiomyocytes in vivo, cardiac morphology and function were assessed in conditional mutant mice.
2017-02-23 | E-MTAB-5441 | biostudies-arrayexpress
Project description:LRRC10 is a heart-specific gene required for proper cardiac function. The effects of Lrrc10 deletion on gene expression in the adult mouse heart was investigated. Lrrc10 knockout mice or wildtype controls, housed in 12 hour light:12 dark, ad lib feeding and drinking conditions were sacrificed at two months of age for cardiac gene expression analysis. A two color, reference design experiment in which heart RNA from 2 Lrrc10 knockout mice was pooled and labeled with Cy5 and hybridized according to Agilent protocols against a reference pool of RNA madeup from respective tissue taken from 2 month wildtype mice which was labeled with Cy3.
2012-03-15 | E-GEOD-36508 | biostudies-arrayexpress
Project description:Gene expression profiles in the heart tissues of heart-specific Bmal1 knockout mice
| PRJNA262134 | ENA
Project description:Transcriptiomics profiling of brown adipose tissue of adipocyte-specific Beclin1 knockout mice
| PRJNA623637 | ENA
Project description:Adult cardiomyocytes (CM) are terminally differentiated cells with minimal regenerative capacity, making cardiac tissue particularly vulnerable to injury. Thus, defining the roadblocks responsible for adult CM cell cycle arrest lies at the core of developing therapies to regenerate myocyte loss following injurious events such as myocardial infarction. We have previously shown that inactivating the p53/Mdm2 tumor suppressor circuitry, specifically in the heart (using the Cre-loxP recombination system of bacteriophage P1), can allow differentiated CMs to regain proliferative capacity, through an upregulation of factors involved in cell cycle re-entry. These factors are repressed in quiescent CMs, in part through the action of microRNAs (miRNAs). Notably, knockout of either p53 or Mdm2 individually was insufficient to promote CM proliferation. Therefore, we hypothesized that inactivation of p53/Mdm2-regulated miRNAs could promote the expression of cell cycle activators and induce proliferation of adult murine CMs. To identify miRNAs regulated by both p53 and Mdm2, total miRNA expression profiles from cardiac specific p53/Mdm2 double knockout (DKO) mouse hearts were compared with those from cardiac-specific single knockouts (p53KO and Mdm2KO), and vehicle-injected controls using the Nanostring nCounter mouse miRNA expression assay. This revealed a profile of 11 significantly downregulated miRNAs in the proliferative DKO hearts (versus vehicle-injected control), that were enriched for mRNA targets involved in cell cycle regulation. In vitro studies have demonstrated that knockdown of these 11 miRNAs in neonatal rat cardiomyocytes can increase the occurrence of cytokinetic events. Ultimately, we aim to inject antagomirs targeting these miRNAs into animals post-myocardial infarction to determine the effect of p53/Mdm2-regulated miRNAs on heart function and CM proliferation in vivo.
2017-03-22 | E-MTAB-5531 | biostudies-arrayexpress
Project description:Mice without cardiac Bmal1 function develop severe progressive heart failure with age. To examine the mechanism underlying the failing heart phenotype observed in heart-specific Bmal1 knockout mice, microarray analyses were performed. The analyses revealed that broad classes of genes regulating cellular energy metabolism were upregulated or downregulated in the heart tissues of heart-specific Bmal1 knockout mice compared with those of control animals.
2014-09-27 | GSE61787 | GEO
Project description:The goal of this study was to gain insight into the molecular heterogeneity of capillary endothelial cells derived from different organs by microarray profiling of freshly isolated cells and identify transcription factors that may determine the specific gene expression profile of endothelial cells from different tissues. The study focused on heart endothelial cells and presents a validated signature of 31 genes that are highly enriched in heart endothelial cells. Within this signature 5 transcription factors were identified and the optimal combination of these transcription factors was determined for specification of the heart endothelial fingerprint. From three tissue types (mouse brain, heart and liver), we collected five freshly isolated endothelial cell samples each. For each brain sample we pooled RNA from 6 mice. For each heart sample we pooled RNA from 4 mice. For each liver sample we pooled RNA from 2 mice. The three endothelial subtypes were then compared. For each subtype, specific gene profiles were defined by determining the genes that were highly enriched versus the other two endothelial subtypes.
2015-02-19 | E-GEOD-48209 | biostudies-arrayexpress