Effects of Dll1 blocking antibody on gene expression profiles of the brachiocephalic arteries in ApoE-deficient mice fed a high-fat diet
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PROVIDER: PRJNA1153006 | ENA |
REPOSITORIES: ENA
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Project description:To examine the effects of Dll1 blocking antibody (Dll1 Ab) on gene expression profiles of the brachiocephalic arteries, ApoE-deficient mice were fed a high-fat diet from 12 weeks of age. Dll1 Ab or control non-immune IgG was intraperitoneally injected from 20 weeks of age. At 32 weeks of age, brachiocephalic arteries were excised, and gene expressions were evaluated.
2025-08-27 | GSE275793 | GEO
Project description:We tried to identify mRNA targets of miR-126 involved in neointima formation in mice with an atherogenic background. Genome-wide expression profiling was carried out in wire-injured carotid arteries of miR-126+/+/ApoE-/- (control group) and miR-126-/-/ApoE-/- (target group) mice on western-type diet. RNA was isolated after 14 days following vascular injury (n=4 each group). Agilent SurePrint G3 Mouse GE Microarrays (8x60K format) were used in combination with a one-color based hybridization protocol. Signals on the microarrays were detected using the Agilent DNA Microarray Scanner. Differential gene expression was identified by applying appropriate biostatistics to the data set. GeneSpring GX11 analysis software was used to normalize and analyze the raw data Genomewide expression profile of miR-126+/+/ApoE-/- and miR-126-/-/ApoE-/- mice were measured at 14 days after vascular injury . 4 animals per group were used.
2014-02-19 | E-GEOD-34262 | biostudies-arrayexpress
Project description:We tried to identify mRNA targets of miR-126 involved in neointima formation in mice with an atherogenic background. Genome-wide expression profiling was carried out in wire-injured carotid arteries of miR-126+/+/ApoE-/- (control group) and miR-126-/-/ApoE-/- (target group) mice on western-type diet. RNA was isolated after 14 days following vascular injury (n=4 each group). Agilent SurePrint G3 Mouse GE Microarrays (8x60K format) were used in combination with a one-color based hybridization protocol. Signals on the microarrays were detected using the Agilent DNA Microarray Scanner. Differential gene expression was identified by applying appropriate biostatistics to the data set. GeneSpring GX11 analysis software was used to normalize and analyze the raw data
2014-02-19 | GSE34262 | GEO
Project description:Objective DLL1 is a mammalian Notch ligand with essential functions during embryonic development. We tagged endogenous DLL1 in one homologous recombination step such that AcGFP-HA tagged DLL1 could be converted by Cre-mediated site-specific recombination into StrepFlag tagged DLL1. We anticipated that this should allow us to visualise DLL1 in living cells as well as allow for sorting and enrichment of DLL1-expressing cells and efficient purification of DLL1 protein complex. Results We generated constructs to express a DLL1 variant that carried C-terminal in frame an AcGFPHA tag flanked by loxP sites followed by a StrepFlag tag out of frame. Cre-mediated recombination removed AcGFP-HA and added StrepFlag in frame to DLL1. The AcGFPHAstopStrepFlag tag was added to the Dll1 cDNA to allow for tests in cultured cells in vitro and was introduced into endogenous DLL1 in mice using ES cells modified by homologous recombination. Tagged DLL1 protein was detected by antibodies against GFP and HA or Flag, respectively, both in CHO cell and embryo lysates. In CHO cells the AcGFP protein fused to DLL1 was functional. In vivo AcGFP expression was below the level of detection by direct fluorescence. However, the StrepFlag tag allowed us to specifically purify DLL1 complexes from embryo lysates. Homozygous mice expressing AcGFPHA or StrepFlag-tagged DLL1 revealed a vertebral column phenotype reminiscent of disturbances in AP polarity during somitogenesis, a process most sensitive to reduced DLL1 function. Thus, even small C-terminal tags can impinge on sensitive developmental processes requiring DLL1 activity.
2021-11-03 | PXD024680 | Pride
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
2008-06-14 | E-GEOD-6134 | biostudies-arrayexpress
Project description:Depletion of cardiac ATP content is a characteristic feature of heart failure in patients and experimental animal models. To analyze the impact of insufficient ATP supply on heart function we inhibited cellular respiration by disulfide poisoning with the mild thiol-blocking agent, cystamine. We chose 4 month-old apolipoprotein E (apoE)-deficient mice, which are highly vulnerable to increased oxygen and ATP demands. After 4 weeks of cystamine treatment (300 mg/kg in drinking water), echocardiography and histology analyses demonstrated that apoE-deficient mice had developed heart failure with cardiac dilation. The microarray gene expression study of heart tissue from cystamine-treated apoE-deficient mice relative to untreated mice confirmed the development of heart failure showing up-regulation heart failure-specific genes by mild thiol-blocking with cystamine. Microarray gene expression profiling was performed with heart tissue isolated from three study groups: (i) cystamine-treated 5 month-old apolipoprotein- (apoE)- deficient mice with symptoms of heart failure, (ii) untreated 5 month-old apoE- deficient mice, and (iii) age-matched, untreated, non-transgenic B6 control mice.
2010-12-03 | E-GEOD-25768 | biostudies-arrayexpress
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. Keywords: Atheroslcersosis development
2007-08-08 | GSE6134 | GEO
Project description:To survey the diverse tumor cell populations of aggressive luminal breast cancer (non-TNBC) at a cellular level, we utilized Dll1+ and Dll1- tumors from a recently published PyMT-Dll1mCherry reporter breast cancer mouse model.
2022-08-14 | GSE182011 | GEO
Project description:Several genes like Nfkb, Npy and Dll1 showed altered enrichment peaks between Dll1+ and Dll1- population of tumor cells.
2020-11-20 | GSE133736 | GEO
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.
2012-12-26 | E-GEOD-26555 | biostudies-arrayexpress