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Genome-wide analysis of gene transcription in myocardium of the doxycycline inducible Tafazzin shRNA knockdown mouse model of Barth syndrome

ABSTRACT: Analysis of the transcriptome of cardiac tissue from mice trangenically engineered with a doxycycline inducible Tafazzin shRNA knockdown to mimic the loss of function of Tafazzin in Barth syndrome. ShRNA induced knockdown mice were compared to wildtype littermates also fed the doxycyline diet. The hypothesis was to investigate adaptive metabolic and compensatory gene transcriptional changes in myocardium of the mouse model of Barth syndrome Total RNA obtained from 2 month old cardiac tissue from the doxycycline inducible shRNA Tafazzin knockdown mouse model of Barth syndrome compared to wildtype littermates also fed 625 mg/Kg doxycycline diet

ORGANISM(S): Mus musculus

SUBMITTER: Michael Kiebish

PROVIDER: E-GEOD-33452 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide analysis of gene transcription in myocardium of the doxycycline inducible Tafazzin shRNA knockdown mouse model of Barth syndrome

Project description:Analysis of the transcriptome of cardiac tissue from mice trangenically engineered with a doxycycline inducible Tafazzin shRNA knockdown to mimic the loss of function of Tafazzin in Barth syndrome. ShRNA induced knockdown mice were compared to wildtype littermates also fed the doxycyline diet. The hypothesis was to investigate adaptive metabolic and compensatory gene transcriptional changes in myocardium of the mouse model of Barth syndrome

2011-11-05 | GSE33452 | GEO

Genome-wide analysis of gene transcription in myocardium of mice transgenically expressing human cardiolipin synthase 1 (hCLS1) in cardiac tissue

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Gene expression altered by high-fructose diet feeding and Chrebp deficiency

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Expression data from Bama minipig hearts - high-fat, high-sucrose diet

Project description:In order to study the heart disorder that the long term, high energy diet caused, Bama miniature pigs were fed a high-fat, high-sucrose diet for 23 months. These pigs developed symptoms of metabolic syndrome and showed cardiac steatosis and hypertrophy with a greatly increased heart weight (1.82-fold, P<0.05) and heart volume (1.60-fold, P<0.05) compared with the control pigs. To understand the molecular mechanisms of cardiac steatosis and hypertrophy, nine pig heart cRNA samples were hybridized to porcine GeneChips. The control group consisted of 6 Bama pigs fed a control diet, and the HFHSD group comprised 6 pigs that were induced with a HFHS diet, which included 37% sucrose, 53% control diet and 10% pork lard. The pigs were fed twice every day and provided water ad libitum for 23 months. The pigs were fasted for 12 hours and euthanized with ketamine and xylazine. Pig hearts from the HFHSD group pigs (120, 126, 138, 140, 144, and 146) and three control group pigs (157, 159, and 161) were sampled and preserved in liquid nitrogen and then for RNA extraction and hybridization on Affymetrix microarrays.

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Expression data from short hairpin RNA mediated CTCF knockdown in human prostate epithelial cells

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