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.
Project description:Affymetrix Microarrays were used to analyse gene expression in aortas and circulating CD115+ cells of ApoE- and ApoE/Lymphotoxin beta receptor (LTbR)-double-deficent mice fed a Western diet from 8 to 12 weeks of age in order to identify regulated genes and pathways leading to reduced atherosclerosis in ApoE-/-/LTbR-/- mice compared to ApoE-/- littermate controls.
Project description:Identification of novel pathways in the development of atherosclerosis. Here, we are looking at changes in gene expression that occur in the aorta with the development of atherosclerosis Analysis used RNA from thoracic aortas from chow fed ApoE knockout mice as control samples for comparison to the experimental samples from 8 week and 16 week ApoE knockout mice fed a western-type diet
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.
Project description:We collected whole genome testis expression data from hybrid zone mice. We integrated GWAS mapping of testis expression traits and low testis weight to gain insight into the genetic basis of hybrid male sterility.
