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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Myocardial gene expression in response to pressure overload

ABSTRACT: Myocardial deletion of klf4 sensitizes mouse to pressure overload. In order to gain a better understanding of molecular mechanisms of such alterations, we profiled gene expression before and after 3-day of pressure overload (induced by transverse aortic constriction -TAC) in the hearts from MHC-cre (Cre) control and MHC-cre-klf4-deficient (KO) mice. 10wk old male mice was subjected to transverse aortic constriction (TAC) to induce pressure overload or sham operation as control group. After 3 days, heart was removed and total RNA was extracted from apex and subjected for array analysis. Four animals in each group.

ORGANISM(S): Mus musculus

SUBMITTER: Mukesh Jain

PROVIDER: E-GEOD-61177 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Myocardial gene expression in response to pressure overload

Project description:Myocardial deletion of klf4 sensitizes mouse to pressure overload. In order to gain a better understanding of molecular mechanisms of such alterations, we profiled gene expression before and after 3-day of pressure overload (induced by transverse aortic constriction -TAC) in the hearts from MHC-cre (Cre) control and MHC-cre-klf4-deficient (KO) mice.

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RNA-Seq analysis of mouse heart tissue

Project description:The purpose of the experiment is to assess the genes expression changes in the heart in response to transverse aortic constriction (TAC)-induced pressure overload, and to identify the genes which are involved in the pathogenesis of heart failure induced by hypertension; thereafter examining the individual gene function in the heart and discovering the novel drug targets to prevent heart failure. Wild-type C57 mice were subjected to transverse aortic constriction (TAC) for 12 weeks (sham as the control, Con). The hearts were collected and snap frozen for the following experiments.

2023-05-23 | E-MTAB-12979 | biostudies-arrayexpress

expression data from Zbtb17 cKO mouse heart after pressure overload

Project description:whole gene expression analysis for ZBTB17 cKO mice after transverse aortic constriction (TAC) We used microarrays to detail the global programme of gene expression underlying hypertrophy and heart failure process upon pressure overload 16 male mice, 4 mice per group, were selected at 8-10 weeks old for 4 weeks of TAC and SHAM and collected samples for RNA extraction and hybridization on Affymetrix microarrays. We included corresponding controls.

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Project description:We analyzed time dependent global proteomic adaptations during heart failure (HF) progression in a mouse model, suffering from left ventricular pressure overload due to transverse aortic constriction (TAC), to gain deeper insights in the disease development and identify new biomarker candidates. The hearts from TAC and sham mice were examined by cardiac MRI on either day 4, 14, 21, 28, 42, and 56 after surgery (n=6 group/time point). At each time point, proteomes of the left (LV) and right ventricles (RV) of TAC and sham mice were analyzed by mass spectrometry (MS).

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Gene and exon expression change in cardiac hypertrophy with pressure overload

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2007-12-01 | E-GEOD-2459 | biostudies-arrayexpress

Gene expression profiles in the hearts of WT and Bcl-xL S14A KI mice after TAC or Sham

Project description:Acute increase of blood pressure by transverse aortic constriction (TAC), pressure overload, stimulates hypertrophic signaling in the heart, which is suppressed in Bcl-xL Ser14Ala knock-in mice.

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mRNA- and RISC-sequencing of mouse hearts overexpressing miR-133a

Project description:miR-133a-3p is a highly abundant cardiomyocyte-enriched microRNA whose expression is persistently decreased in response to pressure overload (or transverse aortic constriction, TAC) in mice. Overexpression of miR-133a in cardiomyocytes of mouse hearts in vivo (under the control of the Myh6 promoter) decreases pressure overload-induced apoptosis and fibrosis. In previous studies using microarray platforms, we detected numerous mRNAs whose transcript levels were altered by either or both of miR-133a overexpression and pressure overload. The data set presented here builds upon our previous study in these mice by examining mRNA-RISC associations (using Ago2-immunoprecipitated RNA) and global mRNA abundances via RNA-sequencing procedures, and tests the hypothesis that mRNAs targeted by overexpressed miR-133a are dissimilar between sham and TAC contexts. Cardiac polyadenylated RNA (mRNA) profiles were generated from nontransgenic and transgenic mouse hearts of FVB/N background, on Illumina HiSeq 2000 instruments. Male mice 8-12 weeks of age were used in these studies, and subjected to sham surgery or 1 week of pressure-overload via transverse aortic constriction (TAC). 3 nontransgenic sham, 7 transgenic sham, 5 nontransgenic TAC, 4 transgenic TAC, each with mRNA-seq and RISC-seq (mRNA-seq of Ago2 immunoprecipitate) data.

2016-01-11 | E-GEOD-65141 | biostudies-arrayexpress

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