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Effect of Activin A on gene expression in atherosclerotic liver in LDLR-/- mice

ABSTRACT: Effect of Activin A on gene expression in atherosclerotic liver in LDLR-/- mice

PROVIDER: PRJNA881390 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21609256_1.fastq.gz	Fastqsanger.gz
	SRR21609256_2.fastq.gz	Fastqsanger.gz
	SRR21609257_1.fastq.gz	Fastqsanger.gz
	SRR21609257_2.fastq.gz	Fastqsanger.gz
	SRR21609258_1.fastq.gz	Fastqsanger.gz

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Effect of Activin A on gene expression in atherosclerotic liver in LDLR-/- mice

Project description:To investigate the mechanism of hepatic Activin A in atherosclerosis, we studied LDLR-/- mice on a Western diet for 12 weeks and used adeno-associated viral vectors with a liver-specific thyroxine binding globulin (TBG) promoter to express Activin A or GFP (control) We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different livers in each group

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Project description:Purpose: The goal of this study was to evaluate the effect of ANGPTL3 inhibition on liver transcriptomes in LDLR KO mice. Methods: Mice were treated once weekly for 3 weeks with 25mg/kg control mAb or ANGPTL3 mAb. Livers were harvested 6 days after the last mAb treatment. Results: ANGPTL3 inhibition had no major impact on hepatic gene expression.

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Project description:Genetic variants at the TRIB1 (Tribbles-homolog 1) gene locus are strongly associated with plasma lipid traits and the risk of coronary artery disease in humans. In this study, we analyzed the consequences of Trib1-deficiency (Trib1-/-) on hepatic gene expression in mice on the atherosclerosis-susceptible LDL-receptor deficient (Ldlr-/-) background. Therefore, Trib1-/- mice were crossed onto the Ldlr-/- background to generate double knockout mice (Trib1-/-Ldlr-/-) and fed a semisynthetic, modified AIN76 diet (0.02% cholesterol, 4.3% fat). At 20 weeks of age, Trib1-/-Ldlr-/- mice and Trib1+/+Ldlr-/- control mice were sacrificed and liver tissue was snap frozen in liquid nitrogen and stored at -80°C until further processing. Total RNA was isolated from liver tissue (n=8 mice per genotype) and subjected to microarray gene expression analysis.

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Project description:The effect of ANGPTL3 mAb on liver transcriptomes in LDLR-deficient mice

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Project description:Inhibition of miR-33 results in increased cholesterol efflux and HDL-cholesterol levels in mice. In this study we examined the effect of miR-33 inhibition in a mouse model of atherosclerosis and observed significant reduction in atherosclerotic plaque size. At the end of the study, gene expression in macrophages from the atherosclerotic plaques was assessed. The results demonstrated a reduction in inflammatory gene expression and increased levels of mRNAs containing miR-33 binding sites. LDLR-/- mice on a Western diet with established atherosclerosis were switched to normal chow and treated with anti-miR-33, control anti-miR, or saline (n=4/group) for 4 weeks. Gene expression profiling was performed on macrophages in aortic plaques isolated at the end of the treatment period by laser capture microdissection.

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