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Altered expression of uc.323 during aortic banding-induced cardiac hypertrophy in mice

ABSTRACT: Altered expression of uc.323 during aortic banding-induced cardiac hypertrophy in mice

PROVIDER: PRJNA592524 | ENA |

REPOSITORIES: ENA

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Altered expression of uc.323 during aortic banding-induced cardiac hypertrophy in mice

Project description:To investigate the changes in T-UCR (transcribed ultraconserved regions) transcription during aortic banding-induced cardiac hypertrophy, we performed lncRNA microarray analysis on the hearts of mice subjected to sham or aortic banding surgery.

2019-11-30 | GSE141165 | GEO

Downstream targets of uc.323-mediated cardiomyocyte hypertrophy

Project description:To further characterize the downstream targets of uc.323, we performed global microarray analysis after knockdown of uc.323 in cardiomyocytes to gain broad insight into uc.323-mediated transcriptome changes.

2019-11-30 | GSE141166 | GEO

Downstream targets of uc.323-mediated cardiomyocyte hypertrophy

Project description:Downstream targets of uc.323-mediated cardiomyocyte hypertrophy

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Transcription profiling of rat heart samples from animals with cardiac hypertrophy induced by aortic banding, myocardial infarction, av-fistula or hormone infusion

Project description:Cardiac hypertrophy was induced by aortic banding (6, 12, 16, and 30 weeks), myocardial infarction (3 and 9 weeks), an av-fistula (aorta abd. to v. cava inf.. 3 and 8 weeks), or hormone infusion (two weeks either angiotensin 2 or a thyroxin analogue). Sham operated or saline infused animals served as controls. Gene expression was determined by Affymetrix RGU34A GeneChip's to identify genes with common regulation in the different models of cardiac hypertrophy.

2007-10-11 | E-GEOD-738 | biostudies-arrayexpress

Transcription profiling of mouse treated by ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium reveals CHF1/Hey2 promotes physiological hypertrophy in response to pressure overload

Project description:We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy. To determine the role of CHF1/Hey2 in pressure overload hypertrophy, we performed ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium. We found that both wild type and transgenic mice developed increased ventricular weight to body weight ratios one week after aortic banding. Wild type mice also developed decreased fractional shortening after one week when compared to preoperative echocardiograms and sham operated controls. Transgenic mice, in comparison, demonstrated preserved fractional shortening. Histological examination of explanted heart tissue demonstrated extensive fibrosis in wild type hearts, but minimal fibrosis in transgenic hearts. TUNEL staining demonstrated increased apoptosis in the wild type hearts but not in the transgenic hearts. Exposure of cultured neonatal myocytes from wild type and transgenic animals to hydrogen peroxide, a potent inducer of apoptosis, demonstrated increased apoptosis in the wild type cells. Gene Set Analysis of microarray data from wild type and transgenic hearts one week after banding revealed suppression and activation of multiple pathways involving apoptosis, cell signaling and biosynthesis. These findings demonstrate that CHF1/Hey2 promotes physiological over pathological hypertrophy in pressure overload through suppression of apoptosis and global regulation of multiple transcriptional pathways. Experiment Overall Design: Ascending aortic banding on four wild type and four transgenic mice were compared

2010-02-17 | E-GEOD-13031 | biostudies-arrayexpress

Altered expression and Downstream targets of uc.323

Project description:Altered expression and Downstream targets of uc.323

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Pressure-Overload Induced Cardiac Hypertrophy

Project description:Aortic banding is an excellent model system to evaluate the process of development of left ventricular hypertrophy in response to hemodynamic stress. The Affymetrix GeneChip MgU74Av1 was used to analyze expression profiles of mice at different time points after surgical intervention for pressure-overload induced hypertrophy. More information about this model may be obtained at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/band_home.html Keywords = Pressure overload, cardiac hypertrophy Keywords: time-course

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The calcineurin splicing variant CnAb1 reduces pressure overload-induced cardiac hypertrophy by promoting mitohormesis

Project description:Analysis of the function of CnAb1 in myocardial hypertrophy in mice using a Gain of Function strategy and Trans Aortic Banding as a hypertrophic stimuly. Microarray was performed after QPCR validation of the upregulation of CnAb1.

2019-03-01 | GSE79536 | GEO

Rat models of cardiac hypertrophy

2004-03-12 | GSE738 | GEO

Expression data from mouse heart after aortic binding surgery for 2 weeks

Project description:We found that tmbim1 is decreased in heart samples from patients with heart failure and in heart tissues from mice with aortic banding (AB)-induced cardiac hypertrophy. Furthermore, deleting Tmbim1 aggravates the AB-induced cardiac hypertrophy. To investigate the potential mechanism by which tmbim1 regulates cardiac hypertrophy, we treated wild type and tmbim1 knockout mice with aortic binding surgery for 2 weeks, and performed microarray to identify the expression pattern and the potential important targets. We used microarrays to detect the global gene expression in the hearts of wild type and Tmbim1 knockout mice after treatment with aortic binding surgery for 2 weeks and identified distinct classes of altered genes

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