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Plaque gene expression out of the aortic root of wildtype (Con) or myeloid-derived lipin-1 KO mice after high fat diet for 8 or 12 weeks

ABSTRACT: Plaque gene expression out of the aortic root of wildtype (Con) or myeloid-derived lipin-1 KO mice after high fat diet for 8 or 12 weeks

PROVIDER: PRJNA637652 | ENA |

REPOSITORIES: ENA

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Plaque gene expression out of the aortic root of wildtype (Con) or myeloid-derived lipin-1 KO mice after high fat diet for 8 or 12 weeks

Project description:mRNA was isolated from aortic root tissue sections isolated from wild type or myeloid-derived lipin-1 knockout (KO) mice on high fat diet and anlyzed for a myeloid innate immunity panel via Canopy Biosciences Nanostring In this study, 750 genes of a myeloid innate immunity panel were analyzed within the aortic root plaques of mice on an atherosclerotic diet to analyze the contributions of lipin-1 to gene expression changes

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Project description:We found that tmbim1 is decreased in heart samples from patients with heart failure and in heart tissues from mice with aortic banding (AB)-induced cardiac hypertrophy. Furthermore, deleting Tmbim1 aggravates the AB-induced cardiac hypertrophy. To investigate the potential mechanism by which tmbim1 regulates cardiac hypertrophy, we treated wild type and tmbim1 knockout mice with aortic binding surgery for 2 weeks, and performed microarray to identify the expression pattern and the potential important targets. We used microarrays to detect the global gene expression in the hearts of wild type and Tmbim1 knockout mice after treatment with aortic binding surgery for 2 weeks and identified distinct classes of altered genes

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Transcriptome profiling of plaque macrophages during atherosclerosis regression

Project description:We have carried out a systems biology investigation of regulators controlling arterial plaque macrophage transcriptional changes in response to lipid lowering, in the Reversa mouse model of plaque regression in which poly I:C injections induce recombination-mediated inactivation of Mttp in the liver and (when combined with a switch to chow diet) restore normal lipid levels in an Ldlr-/-Apob100/100 mouse (Lieu et al., 2003, Circulation, v.107(9), pp.1315-21). Twenty-four Reversa mice (12 males, 12 females) were maintained on Western diet for 16 weeks and given injections of either poly I:C or vehicle (saline) and then switched to normal chow. At seven days after the last injection, animals were sacrificed and CD68+ macrophages were isolated from the aortic root plaque using laser-capture microdissection. An additional two Ldlr-/- animals (male) were treated with poly I:C and CD68+ aortic root plaque macrophages were obtained, as a control group for effects of poly I:C independent of Mttp inactivation. RNA isolated from each of the 26 samples was reverse-transcribed, amplified, fragmented, labeled, and then hybridized to the Affymetrix Mouse Exon Array 1.0 ST GeneChip. Probe intensities were analyzed using transcript-level probesets for gene expression profiling, and for each mouse transcript represented on the microarray, a two-factor model (sex and treatment) was used for the analysis of the 24 samples from the Reversa mice, to test for a significant effect of the poly I:C (vs. saline) treatment.

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Sclerostin Antibody Does Not Promote Atheroprogression, Plaque Mineralization, or Inflammation in Ovariectomized Apolipoprotein E–Deficient Mice

Project description:Objective—Overexpression or administration of sclerostin has been reported to have atheroprotective and anti-inflammatory effects in apolipoprotein E knockout (ApoE KO) mice infused with angiotensin II; however, effects of sclerostin inhibition on these processes are not known. This study examined the effects of sclerostin inhibition with a sclerostin antibody on transcriptional changes in the aortic arch, associated morphological changes in aortic atherosclerotic plaques, and circulating markers of inflammation in ApoE KO ovariectomized (OVX) mice fed a high-fat diet. Approach and Results—Sclerostin antibody or vehicle was administered by subcutaneous injection once weekly for 3, 8, or 16 weeks to ApoE KO-OVX and wild-type-OVX mice fed a high-fat diet. As a comparator, alendronate or saline was administered twice weekly for 16 weeks to ApoE KO-OVX mice fed a high-fat diet. Sclerostin antibody had no effect on aortic total or mineralized plaque volume, determined by microcomputed tomography. Sclerostin antibody had no meaningful effects on plaque histopathology or systemic markers of inflammation or endothelial/platelet activation. Transcriptional analysis of the aortic arch revealed significant gene expression and signaling pathway changes in ApoE KO mice compared with wild-type, consistent with the genotype and atheroprogression, that were not affected by sclerostin antibody treatment. Alendronate treatment did not alter plaque volume or histopathology. Conclusions—This study shows that inhibition of sclerostin by sclerostin antibody does not promote atheroprogression or affect systemic markers of inflammation in the high-fat diet ApoE KO-OVX mouse model and does not alter the expression of genes/pathways implicated in atherosclerosis.

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Project description:Klotho-deficient mice develop aortic valve annulus calcification by 6 weeks of age. Understanding the molecular basis by which aortic valve calcification is initiated will help define potential molecular targets which may be inhibited to reduce or prevent aortic valve calcification. Changes in gene expression related to aortic valve annulus calcification were analyzed by comparing gene expression in the aortic roots from wild type versus klotho-deficient mice.

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Aortic macrophages and endothelial cells of apoE KO mice aortas after plaque regression induced apoE adenoviral transfer

Project description:Aortic macrophages and endothelial cells of apoE KO mice were sorted and analyzed by microarray 2 weeks after regression was induced by adenoviral transfer of apoE.

2015-01-01 | GSE42691 | GEO

Aortic macrophages and endothelial cells of apoE KO mice aortas after plaque regression induced apoE adenoviral transfer

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