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MiRNAs expression profile in ischemic hindlimb muscle of normocholesterolemic (C57) vs hypercholesterolemic (Apoe-/-) mice.

ABSTRACT: miRNAs expression profile in ischemic hindlimb muscle of normocholesterolemic (C57) vs hypercholesterolemic (Apoe-/-) mice.

PROVIDER: PRJNA542269 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9040296_1.fastq.gz	Fastqsanger.gz
	SRR9040296_2.fastq.gz	Fastqsanger.gz
	SRR9040297_1.fastq.gz	Fastqsanger.gz
	SRR9040297_2.fastq.gz	Fastqsanger.gz

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miRNAs expression profile in ischemic hindlimb muscle of normocholesterolemic (C57) vs hypercholesterolemic (Apoe-/-) mice.

Project description:Using NGS, we report the differential-expression profiling of miRNAs in hypercholesterolemic/atherosclerotic conditions in hindlinb ischemic muscle compare to healthy control mice. Data of total miRNA expression are presented as normalized copy number: read per millions of read (RPM). Hindlimb ischemia was surgicaly induced by feromal artery ablation and the animal was sacrified 1 day after surgery for RNA collection.

2019-05-11 | GSE131002 | GEO

Transcription profiling of mouse offspring of crosses between hypercholesterolemic and normocholesterolemic parents LUMC-HKG-ApoE-Atherosclerosis

Project description:Enhanced prenatal fatty streak formation in human fetuses has been associated with maternal hypercholesterolemia. However, the possible roles of maternal genetic background and in utero environment on development of atherosclerosis in adult life have not been unraveled. We generated genetically identical heterozygous apoE-deficient mice offspring with a different maternal background to study the intrauterine effect of maternal genotype and associated hypercholesterolemia on the developing vascular system. As read out for increased atherosclerosis development in adult life, a constrictive collar was placed around the carotid artery to induce lesion formation. A significant increase in endothelial cell activation and damage was detected in the carotid arteries of heterozygous apoE-deficient fetuses with apoE-deficient mothers compared with offspring from wild type mothers, but no fatty streak formation was observed. Postnatally, all carotid arteries revealed normal morphology. In adult offspring with maternal apoE-deficiency, the constrictive collar resulted in severe lesion (9/10) development compared with no to only minor lesions (2/10) in offspring of wild type mothers. Microarray analysis showed no effect of maternal apoE-deficiency on gene expression in adult offspring. We conclude that maternal apoE-deficiency not only affects fetal arteries, but also increases the susceptibility for development of collar-induced atherosclerosis in adult life. Experiment Overall Design: Crossing of hypercholesterolemic female with normocholesterolemic male and vice versa, determination of susceptabilioty to atherosclerosis in offspring

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Transcriptome analysis of CD45-CD31+ endothelial cells in ischemic hindlimb muscle after IL-35 injection

Project description:We report the first time of the transcriptome difference between IL35- and PBS-injected ischemic muscle after hindlimb ischemia, specifically in isolated CD45-CD31+ endothelial cell

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Cardiac gene expression profiling of apoE-deficient mice receiving heart failure treatment with the anti-ischemic drug ranolazine

Project description:Heart failure is a leading cause of cardiovascular mortality with limited options for treatment. We used 18 month-old apolipoprotein E (apoE)- deficient mice as a model of atherosclerosis-induced heart failure to analyze whether the anti-ischemic drug ranolazine could retard the progression of heart failure. The study showed that 2 months of ranolazine treatment improved cardiac function of 18 month-old apoE-deficient mice with symptoms of heart failure as assessed by echocardiography. To identify changes in cardiac gene expression induced by treatment with ranolazine a microarray study was performed with heart tissue from failing hearts relative to ranolazine-treated and healthy control hearts. The microarray approach identified heart failure-specific genes that were normalized during treatment with the anti-ischemic drug ranolazine. Microarray gene expression profiling was performed with heart tissue isolated from (i) untreated 18 month-old apoE-deficient mice with heart failure relative to (ii) 18 month-old apoE-deficient mice treated for two months with the anti-ischemic drug ranolazine (200 mg/kg), and (iii) age-matched non-transgenic C57BL/6J (B6) control mice.

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Offsprings of crosses between hypercholesterolemic and normocholesterolemic parents LUMC-HKG-ApoE-Atherosclerosis

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Cardiac gene expression profiling of apoE-deficient mice receiving heart failure treatment with the anti-ischemic drug ranolazine

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Microarray gene expression profiling of aorta genes of APOE-deficient mice receiving the ACE inhibitor captopril

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Transcription profiling of mouse aorta genes of APOE-deficient animals receiving the ACE inhibitor captopril

Project description:Microarray gene expression profiling of aorta genes of APOE-deficient mice receiving atherosclerosis treatment with the ACE inhibitor captopril. Hypercholesterolemic APOE-deficient mice were used as a standard model of atherosclerosis to study gene expression changes during atherosclerosis treatment with the ACE inhibitor captopril. Microarray analysis was performed of whole aortas isolated from captopril-treated APOE-deficient mice relative to untreated APOE-deficient mice with overt atherosclerosis, and nontransgenic control mice. Microarray gene expression profiling revealed that captopril-mediated atherosclerosis prevention involved inhibition of aorta-infiltrating immune cells such as pro-atherogenic T lymphocytes and macrophages. Experiment Overall Design: Microarray gene expression profiling was performed of whole aortas isolated from APOE-deficient mice with atherosclerosis relative to captopril-treated APOE-deficient mice, and nontransgenic control mice. Three study groups were analyzed, i.e. 8-months-old untreated APOE-deficient mice with overt atherosclerosis, age-matched APOE-deficient mice treated for 7 months with the angiotensin-converting enzyme (ACE) inhibitor, captopril (20 mg/kg in drinking water), and nontransgenic control C57BL/6J mice. Two biological replicates were made of each group, and total RNA of three aortas was pooled for one gene chip.

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Sex differences in statin response in hypercholesterolemic (Apoe knockout) Four Core Genotypes mice.

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