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Changes in the expression of miRs in the aorta after 3 and 10 months of a high fat diet compared with normal diet

ABSTRACT: We tried to identify miRs that are differentially expresssed during atherogenesis. Aortic miRs expression profile in female apoe-/- mice after 3 and 10 months of a high fat diet were compared with female apoe-/- mice on normal diet.

ORGANISM(S): Mus musculus

PROVIDER: GSE26557 | GEO | 2014/01/01

SECONDARY ACCESSION(S): PRJNA142111

REPOSITORIES: GEO

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Changes in the expression of miRs in the aorta after 3 and 10 months of a high fat diet compared with normal diet

Project description:We tried to identify miRs that are differentially expresssed during atherogenesis. Aortic miRs expression profile in female apoe-/- mice after 3 and 10 months of a high fat diet were compared with female apoe-/- mice on normal diet. 4 Female apoe-/- mice (6-8 weeks) were fed on high fat diet for 3 months. 3 female apoe-/- mice (6-8 weeks) were fed on high fat diet for 10 months. 4 female apoe-/- mice (6-8 weeks) on normal diet served as controls. Total RNA was isolated from whole aortic tissue. RNA samples with RIN>8 were used for array. The aortic miRs expression profile after 3 months of a high fat diet was compared with the control group. Biological replicates: 4 per group. One replicate per array.

2014-01-01 | E-GEOD-26557 | biostudies-arrayexpress

Changes in miR expression profile carotid plaques induced by acutely induced flow disturbances in apoe-/- mice on a high fat diet.

Project description:Atherosclerosis is causally related to disturbed flow through low and oscillatory shear stress. In order to study the miR expression profile in atherosclerotic plaques induced by disturbed flow, partial ligation of the carotid artery was performed. This procedure results acutely in severly reduced blood flow and in stenotic lesion formation within 6 weeks in apoe-/- mice on a high fat diet. We compared the miR expression profile in partially ligated left carotid arteries with the untreated right carotid artery to identify miRs which are involved in plaque formation through flow disturbances. The left carotid arteries of 6 female apoe-/- mice (6-8 weeks) were partially ligated (i.e. the external and internal carotid artery as well as the occipital artery were occluded; blood flow out of the common carotid artery occurs mainly through the superior thyroid artery). Following partial ligation the animals were fed a high fat diet for 6 weeks. Total RNA was isolated from partially ligated left carotid arteries and untreated right carotid arteries (control). MiRs expression profile of the partially ligated carotid arteries were compared with the control group. Biological replicates: 6 per group. One replicate per array.

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Project description:Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder that is influenced by genetic and environmental risk factors, such as inheritance of ε4 allele of APOE (APOE4), sex and diet. Here, we examined the effect of high fat diet (HFD) on amyloid pathology and expression profile in brains of AD model mice expressing human APOE isoforms (APP/E3 and APP/E4 mice). APP/E3 and APP/E4 mice were fed HFD or Normal diet for 3 months. We found that HFD significantly increased amyloid plaques in male and female APP/E4, but not in APP/E3 mice. To identify differentially expressed genes and gene-networks correlated to diet, APOE isoform and sex, we performed RNA sequencing and applied Weighted Gene Co-expression Network Analysis. We determined that the immune response network with major hubs Tyrobp/DAP12, Csf1r, Tlr2, C1qc and Laptm5 correlated significantly and positively to the phenotype of female APP/E4-HFD mice. Correspondingly, we found that in female APP/E4-HFD mice, microglia coverage around plaques, particularly of larger size, was significantly reduced. This suggests altered containment of the plaque growth and sex-dependent vulnerability in response to diet. The results of our study show concurrent impact of diet, APOE isoform and sex on the brain transcriptome and AD-like phenotype.

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