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Transcriptome profiling of murine aortic Vascular Smooth Muscle cells from ApoE knockout and ApoE/Neil3 double knockout mice

ABSTRACT: We performed high-throughput RNA sequencing to characterize possible differences in the transcriptome of murine aortic Vascular Smooth Muscle cells from both 26 weeks-old ApoE knockout and ApoE/Neil3 double knockout mice fed a regular diet.

ORGANISM(S): Mus musculus

PROVIDER: GSE140790 | GEO | 2021/03/15

REPOSITORIES: GEO

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Transcriptome profiling of murine aortic Vascular Smooth Muscle cells from ApoE knockout and ApoE/Neil3 double knockout mice

Project description:Transcriptome profiling of murine aortic Vascular Smooth Muscle cells from ApoE knockout and ApoE/Neil3 double knockout mice

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Transcriptome profiling of primary human aortic Vascular Smooth Muscle cells abrogated of NEIL3 mRNA via antisense oligonucleotides targeting NEIL3 exon 4

Project description:We performed high-throughput RNA sequencing to characterize possible differences in the transcriptome of primary human aortic Vascular Smooth Muscle cells abrogated of NEIL3 mRNA via antisense oligonucleotides targeting NEIL3 exon 4, compared with control cells treated with a scramble version of the same antisense oligonucleotide

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Expression data from ADORA1 knockout and ADORA1 APOE double-knockout mice

Project description:The goal of this study is to determine whether A1 adenosine receptor (ADORA1) plays a role in atherosclerosis development and its possible mechanisms. This dataset compares gene expression (aortas) of ADORA1 knockout mice to ADORA1+APOE double-knockout mice. Mice deficient in both ADORA1 and APOE (DKO) demonstrated reduced atherosclerotic lesions in aortic arch (en face), aortic root, and innominate arteries when compared to (APOE-KO) of the same age. Treating APOE-KO with the ADORA1 antagonist DPCPX also achieved concentration-dependent reduction in lesions. The total plasma cholesterol and triglyceride levels were not different between DKO and APOE-KO, however, higher triglyceride was observed in DKO fed a high-fat diet. DKO also were heavier than APOE-KO. Plasma cytokine levels (IL-5, IL-6, and IL-13) were significantly lower in DKO. Proliferating cell nuclear antigen (PCNA) expression was also significantly reduced in the aorta from DKO. Despite smaller lesions in DKO, the composition of the innominate artery lesions and cholesterol loading and effusion [export] from bone-marrow-derived macrophages from DKO were not different from APOE-KO.

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Expression data from the aortas of ApoE knockout, ApoE/Caspase-1 double knockout, and wild-type mice

Project description:Caspase-1 activation senses metabolic danger-associated molecular patterns and mediates the initiation of inflammation. Here, we reported that caspase-1 contributes to hyperlipidemia-induced modulation of vascular cell gene expression during early atherosclerosis in vivo. Our results demonstrate the therapeutic potential of caspase-1 inhibition in the treatment of cardiovascular diseases. All mice were in a C57B/L6 strain background. Male wild-type mice, Apolipoprotein E (ApoE) gene knockout mice, and ApoE/Caspase-1 double gene deficient mice were fed with high fat diet for 3 weeks starting from 8 weeks to induce early dyslipidemia. At 11-week of age, aortas from these mice were used for microarray analysis. 5 biological replicates in each group.

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Aortic arch profiling of Apoe knockout mice

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Aortic arch profiling of Apoe knockout mice

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Project description:The physiological functions other than lipid metabolism of APOE may interfere with the research results of Apoe-knockout mice as atherosclerosis models. The elucidation of the molecular basis of the physiological functions of APOE other than lipid metabolism will help to make rational use of the Apoe-knockout mouse model. Therefore, our aim is to reveal the changes in aortic gene expression profile caused by Apoe-knockout. We used the second generation sequencing to detect the gene mRNA expression level in the aortic tissues of 5 C57BL/6J mice and 4 Apoe knockout mice. This will provide more clues for studying the physiological function of Apoe, and also remind researchers to pay special attention to the possible interference to the results when using Apoe-knockout mice as atherosclerosis models.

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