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Transient ACE Inhibition Suppresses Future Fibrogenic Capacity and Heterogeneity of Cardiac Fibroblast Subpopulations

ABSTRACT: Transient ACE Inhibition Suppresses Future Fibrogenic Capacity and Heterogeneity of Cardiac Fibroblast Subpopulations

PROVIDER: PRJNA655239 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12389100.fastq.gz	Fastqsanger.gz
	SRR12389101.fastq.gz	Fastqsanger.gz
	SRR12389102.fastq.gz	Fastqsanger.gz
	SRR12389103.fastq.gz	Fastqsanger.gz
	SRR12389104.fastq.gz	Fastqsanger.gz

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Transient ACE Inhibition Suppresses Future Fibrogenic Capacity and Heterogeneity of Cardiac Fibroblast Subpopulations

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

Transient ACE (Angiotensin-Converting Enzyme) Inhibition Suppresses Future Fibrogenic Capacity and Heterogeneity of Cardiac Fibroblast Subpopulations.

Project description:Transient ACE (angiotensin-converting enzyme) inhibition in spontaneously hypertensive rats is known to protect against future injury-induced cardiac inflammation, fibrosis, and dysfunction; however, the mechanisms of protection have not been delineated. Here, we used single-cell RNA sequencing to test the hypothesis that transient ACE inhibitor treatment would induce a persistent shift in cardiac fibroblast subpopulations. Adult male spontaneously hypertensive rats (11 weeks old, hypertensive with cardiac hypertrophy) were treated for 2 weeks with an ACE inhibitor, enalapril (30 mg/kg per day, PO), or water (untreated spontaneously hypertensive rats) followed by a 2-week washout period (n=7/group). Cardiac fibroblasts were isolated from the left ventricle and subjected to single-cell RNA sequencing. Nine clusters of fibroblasts were identified, with 98% of cells in clusters 0 to 6. The transient treatment produced significant changes both within and across clusters. Cluster 1 depicted a 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 (eg, COL1A1, COL3A1, and FN1; all P<1×10-35). Clusters 2 to 5 reflected proliferative, moderately fibrogenic, translationally active, and less inflammatory subsets of fibroblasts, all of which exhibited 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.

| S-EPMC7878436 | biostudies-literature

RNA-Sequencing Quantitative Analysis of Mice Wild Type and Tg-ACE (ACE overexpression) Macrophages

Project description:In this study we compared transcriptome profiling (RNA-seq) in wild type vs. ACE overexpressiong Tg-ACE macrophages to identify differential gene expression/pathways.

2019-01-18 | GSE123952 | GEO

ACE

Project description:Oryctolagus cuniculus ACE, Oryctolagus cuniculus angiotensin I converting enzyme (ACE), transcript variant 2, mRNA. [Source:RefSeq mRNA;Acc:NM_001171069], is expressed in 1 baseline experiment(s);

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Ace

Project description:Drosophila melanogaster Ace, Acetylcholine esterase, is expressed in 4 baseline experiment(s);

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Ace

Project description:Drosophila melanogaster Ace, Acetylcholine esterase, is differentially expressed in 15 experiment(s);

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Hippocampal gene expression profiling of a model of Alzheimer`s Disease upon treatment with the ACE inhibitor captopril

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

ACE-inhibition induces a cardioprotective transcriptional response in the metabolic syndrome heart.

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

Angiotensin Converting Enzyme (ACE) expression in microglia reduces amyloid β deposition and neurodegeneration by increasing SYK signaling and endolysosomal trafficking.

Project description:Angiotensin Converting Enzyme (ACE) has been studied for its role in the regulation of myeloid cell bactericidal and antitumor activity. Here, we generated a mouse model with Tamoxifen-dependent ACE expression with Cx3CR1-Cre control. These mice were crossed to 5xFAD and 9 month forebrains were harvested for their nuclei to assess the ACE-dependent changes in amyloid-reactive microglia.

2025-03-24 | GSE288410 | GEO

Angiotensin Converting Enzyme (ACE) expression in microglia reduces amyloid β deposition and neurodegeneration by increasing SYK signaling and endolysosomal trafficking

Project description:Angiotensin Converting Enzyme (ACE) has been studied for its role in the regulation of myeloid cell bactericidal and antitumor activity. Here, we generated a mouse model with Tamoxifen-dependent ACE expression and Cx3CR1-Cre control. These mice were crossed to 5xFAD and 9 month forebrains were harvested and FFPE processed to assess the ACE-dependent changes in amyloid-reactive microglia.

2025-03-24 | GSE288280 | GEO

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