RNA-Sequencing Quantitative Analysis of Mice Wild Type and Tg-ACE (ACE overexpression) Macrophages
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE123952 | GEO | 2019/01/18
REPOSITORIES: GEO
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Project description:RNA-Sequencing Quantitative Analysis of Mice Wild Type and Tg-ACE (ACE overexpression) Macrophages
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Project description:Macrophages mediate key antimicrobial responses against intracellular bacterial pathogens, such as Salmonella enterica. Yet, they can also act as a permissive niche for these pathogens to persist in infected tissues within granulomas, which are immunological structures comprised of macrophages and other immune cells. We apply single-cell transcriptomics to investigate macrophage functional diversity during persistent Salmonella enterica serovar Typhimurium (STm) infection in mice. We identify determinants of macrophage heterogeneity in infected spleens and describe populations of distinct phenotypes, functional programming, and spatial localization. Using a STm mutant with impaired ability to polarize macrophage phenotypes, we find that angiotensin converting enzyme (ACE) defines a granuloma macrophage population that is non-permissive for intracellular bacteria and their abundance anticorrelates with tissue bacterial burden. Disruption of pathogen control by neutralizing TNF is linked to preferential depletion of ACE+ macrophages in infected tissues. Thus ACE+ macrophages have limited capacity to serve as cellular niche for intracellular bacteria to establish persistent infection.
2022-10-20 | GSE215880 | GEO
Project description:Thymic microRNA expression profiles of wild type vs Tat-Transgenic mice Wild type vs HIV-1 Tat Transgenic mice - microRNA Expression: 3 Biological Replicates The overall experiment included 3 Chip: 1) Wild -type BDF-1 (Cy3) vs F33-Tat-Tg mice (Cy5); 2) F33-Tat-Tg mice (Cy3) vs Wild -type BDF-1 (Cy5); 3) Wild -type BDF-1 (Cy3) vs F33-Tat-Tg mice (Cy5)
2015-07-06 | E-GEOD-65006 | biostudies-arrayexpress
Project description:The goal of the current study was to characterize the cardiac transcriptional signature of the metabolic syndrome (MetS) murine model relative to the healthy, control heart and the differential changes induced by ACE-inhibition, a frequent intervention in MetS subjects, at the transcriptomic level in control and MetS hearts. Methods - LDLR-/-;ob/ob (DKO, MetS model) and C57Bl6/J (WT) mice were injected with ACE-inhibitor captopril (10 mg/kg/day) between 12 and 24 weeks of age, or NaCl 0,9% as controls. Transcriptome analysis (RNA-seq) from the whole heart RNA samples was performed. Differential gene expression was analysed with Cufdiff. Ingenuity Pathway Analysis (IPA) was used to determine functional enrichment, and analyse pathways, networks, and upstream regulators. Transcription factor motif enrichment analysis was performed with i-cisTarget. Results – 288 genes implicating 72 pathways were differentially expressed between DKO and WT hearts. The hallmarks of MetS in the heart were an increase in activity of the following pathways: ILK, Rho, dendritic cell maturation, production of nitric oxide and reactive oxygen species in macrophages, atherosclerosis, LXR-RXR, cardiac hypertrophy, and acute phase response. ACE-inhibition resulted in a limited transcriptional effect in WT hearts and in a decrease in activity of Rho-associated signalling pathways. In contrast, a more prominent transcriptional effect was observed in DKO hearts. Similar to WT, Rho-associated pathways were affected, but ACE-inhibition further displayed a counteracting effect on the pathways affected by MetS in the heart Conclusion –MetS and control mouse hearts have unique transcriptional profiles, with characteristic baseline gene expression landscapes prior to ACE-inhibition, and a partially specific transcriptional response to ACE-inhibition. The Rho-associated signalling pathways and Rho, Rock, Myl, and Fos genes represent potential therapeutic targets.
2018-11-14 | GSE112975 | GEO
Project description:Microarray gene expression profiling of aorta genes of APOE-deficient mice receiving atherosclerosis treatment with the ACE inhibitor captopril. Hypercholesterolemic APOE-deficient mice were used as a standard model of atherosclerosis to study gene expression changes during atherosclerosis treatment with the ACE inhibitor captopril. Microarray analysis was performed of whole aortas isolated from captopril-treated APOE-deficient mice relative to untreated APOE-deficient mice with overt atherosclerosis, and nontransgenic control mice. Microarray gene expression profiling revealed that captopril-mediated atherosclerosis prevention involved inhibition of aorta-infiltrating immune cells such as pro-atherogenic T lymphocytes and macrophages.
2009-12-03 | GSE19286 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare two hepatic macrophage subsets in wild-type (WT) mice with TG mice transcriptome profiling (RNA-seq).
2022-10-31 | GSE186712 | GEO
Project description:Microarray gene expression profiling of aorta genes of APOE-deficient mice receiving atherosclerosis treatment with the ACE inhibitor captopril. Hypercholesterolemic APOE-deficient mice were used as a standard model of atherosclerosis to study gene expression changes during atherosclerosis treatment with the ACE inhibitor captopril. Microarray analysis was performed of whole aortas isolated from captopril-treated APOE-deficient mice relative to untreated APOE-deficient mice with overt atherosclerosis, and nontransgenic control mice. Microarray gene expression profiling revealed that captopril-mediated atherosclerosis prevention involved inhibition of aorta-infiltrating immune cells such as pro-atherogenic T lymphocytes and macrophages. Experiment Overall Design: Microarray gene expression profiling was performed of whole aortas isolated from APOE-deficient mice with atherosclerosis relative to captopril-treated APOE-deficient mice, and nontransgenic control mice. Three study groups were analyzed, i.e. 8-months-old untreated APOE-deficient mice with overt atherosclerosis, age-matched APOE-deficient mice treated for 7 months with the angiotensin-converting enzyme (ACE) inhibitor, captopril (20 mg/kg in drinking water), and nontransgenic control C57BL/6J mice. Two biological replicates were made of each group, and total RNA of three aortas was pooled for one gene chip.
2009-12-14 | E-GEOD-19286 | biostudies-arrayexpress
Project description:Transient angiotensin converting enzyme (ACE) inhibition in spontaneously hypertensive rats (SHR) protects against future injury-induced cardiac inflammation, fibrosis, and dysfunction. Here, we used single cell RNA sequencing (scRNA-Seq) to test the hypothesis that transient ACE inhibitor treatment would induce a persistent shift in hypertensive cardiac fibroblast subpopulations. Adult male SHRs (11 weeks old) were treated for 2 weeks with an ACE inhibitor, enalapril (30mg/kg/day, p.o.), or water (control) followed by a 2-week washout period (n=7/group). Cardiac fibroblasts were isolated from the left ventricle and subjected to scRNA-Seq. Nine clusters of fibroblasts (numbered 0-8) were identified with 98% of cells clustering into subsets 0-6. Transient treatment produced significant changes within and across clusters. Cluster 1 depicted the highly fibrogenic gene profile, with cluster 6 serving as a gateway to cluster 1. Transient ACE inhibition depleted the gateway and expanded cluster 0, which was the least fibrogenic profile. Moreover, within cluster 1 fibroblasts, ACE inhibition reduced expression of individual fibrosis genes (e.g. COL1A1, COL3A1, and FN1; all p<0.05). Clusters 2-5 reflected proliferative, moderately fibrogenic, translationally active, and lowly inflammatory subsets of fibroblasts, all of which exhibit attenuated fibrogenic gene expression after transient ACE inhibition. In conclusion, transient ACE inhibition shifts cardiac fibroblast subpopulations and degree of activation resulting in an overall reduced fibrogenic phenotype.
2020-10-01 | GSE155699 | GEO
Project description:EP4-Tg aortic VSMCs: Control vs PGE2
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Project description:Extracellular senile plaques of amyloid beta (Abeta) are a pathological hallmark in brain of patients with Alzheimer`s Disease (AD). Abeta is generated by the amyloidogenic processing of the amyloid precursor protein (APP). Concomitant to Abeta load, AD brain is characterized by an increase in protein level and activity of the angiotensin-converting enzyme (ACE). ACE inhibitors are a widely used class of drugs with established benefits for patients with cardiovascular disease. However, the role of ACE and ACE inhibition in the development of Abeta plaques and the process of AD-related neurodegeneration is not clear since ACE was reported to degrade Abeta. To investigate the effect of ACE inhibition on AD-related pathomechanisms, we used Tg2576 mice with neuron-specific expression of APPSwe as AD model. From 12 months of age, substantial Abeta plaque load accumulates in the hippocampus of Tg2576 mice as a brain region, which is highly vulnerable to AD-related neurodegeneration. The effect of central ACE inhibition was studied by treatment of 12 month-old Tg2576 mice for six months with the brain penetrating ACE inhibitor captopril. At an age of 18 months, hippocampal gene expression profiling was performed of captopril-treated Tg2576 mice relative to untreated 18 month-old Tg2576 controls with high Abeta plaque load. As an additional control, we used 12 month-old Tg2576 mice with low Abeta plaque load. Whole genome microarray gene expression profiling revealed gene expression changes induced by the brain-penetrating ACE inhibitor captopril, which could reflect the neuro-regenerative potential of central ACE inhibition.
2013-05-14 | GSE46871 | GEO