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Macrophage extracellular traps originated from the vascular smooth muscle cells play key roles in atherosclerosis progression [scRNA-seq]

ABSTRACT: Macrophage extracellular traps originated from the vascular smooth muscle cells play key roles in atherosclerosis progression [scRNA-seq]

PROVIDER: PRJNA808770 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18083476_1.fastq.gz	Fastqsanger.gz
	SRR18083476_2.fastq.gz	Fastqsanger.gz
	SRR18083477_1.fastq.gz	Fastqsanger.gz
	SRR18083477_2.fastq.gz	Fastqsanger.gz
	SRR18083478_1.fastq.gz	Fastqsanger.gz

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Macrophage extracellular traps originated from the vascular smooth muscle cells play key roles in atherosclerosis progression.

Project description:Macrophage extracellular traps originated from the vascular smooth muscle cells play key roles in atherosclerosis progression.

| PRJNA808764 | ENA

Macrophage extracellular traps originated from the vascular smooth muscle cells play key roles in atherosclerosis progression [RNA-seq]

Project description:Macrophage extracellular traps originated from the vascular smooth muscle cells play key roles in atherosclerosis progression [RNA-seq]

| PRJNA808769 | ENA

Macrophage extracellular traps originated from the vascular smooth muscle cells play key roles in atherosclerosis progression [scRNA-seq]

Project description:Smooth muscle cells (SMC) play significant roles in atherosclerosis via phenotypic switching, a pathological process in which SMC transdifferentiation into macrophage-like SMCs. Furthermore, during transdifferentiation, the SMCs' expression of PADI4 upregulating and SMC generated extracellular trap, a web-like structure, which plays key role in the development of atherosclerosis plaque. To reveal the function of SMC's generating ETs during atherosclerosis and to identify molecular targets for disease therapy, we combined SMC fate mapping and single-cell RNA sequencing of mouse atherosclerotic plaques.

2022-11-04 | GSE197073 | GEO

Macrophage extracellular traps originated from the vascular smooth muscle cells play key roles in atherosclerosis progression [RNA-seq]

Project description:Smooth muscle cells (SMC) play significant roles in atherosclerosis via phenotypic switching, a pathological process in which SMC transdifferentiation into macrophage-like SMCs. Furthermore, during transdifferentiation, the SMCs' expression of PADI4 upregulating and SMC generated extracellular trap, a web-like structure, which plays key role in the development of atherosclerosis plaque. To reveal the potential mechanism of the SMC derived macrophages generated ETs surducing surrounding SMCs within the media of artery during the process of atherosclerosis plaque development, we utilized the dsDNA and H3CIT protein to stimuli the SMCs, the SMC stimulated with 0.2%BSA as coontrol group, we collect the cells and did RNA-sequencing between two groups to find the potential signaling pathway participating in the process

2022-11-04 | GSE197074 | GEO

Macrophage extracellular traps originated from the vascular smooth muscle cells play key roles in atherosclerosis progression.

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-11-04 | GSE197075 | GEO

Transcription profiling of mouse smooth muscle cells in atherosclerosis-prone and resistant regions of aorta

Project description:This SuperSeries is composed of the following subset Series:; GSE13835: Smooth muscle cells in atherosclerosis-prone and resistant regions of the aorta of C57Bl/6 mice at age of 4 months; GSE13836: Smooth muscle cells in atherosclerosis-prone and resistant regions of the aorta of apoE-/- mice at age of 4 months Experiment Overall Design: Refer to individual Series

2009-05-27 | E-GEOD-13865 | biostudies-arrayexpress

Neutrophil Extracellular Traps (NETs) promote macrophage inflammation and impair atherosclerosis resolution in mice with diabetes

Project description:Neutrophil extracellular traps (NETs) promote inflammation and atherosclerosis progression. In diabetes they are increased and impair wound healing, during which inflammation normally resolves. Atherosclerosis regression, a process resembling wound healing, is also impaired in diabetes. Thus, we hypothesized that NETs impede atherosclerosis regression in diabetes through unresolved inflammation. Objective: To investigate in diabetes the effect of NETs on plaque macrophage inflammation and whether NETs reduction improves atherosclerosis regression. Findings: Transcriptomic profiling of plaque macrophages from NET positive and negative areas in Ldlr-/- mice revealed inflammasome and glycolysis pathway upregulation, indicating a pro-inflammatory phenotype. During atherosclerosis regression in non-diabetic mice, plaque NET content decreased. In contrast, in diabetic mouse plaques NETs were enriched and persisted after lipid-lowering. DNase1 treatment (to degrade NETs) of diabetic mice reduced plaque NETs and macrophage inflammation and improved atherosclerosis regression after lipid-lowering. Conclusions: NETs decline during atherosclerosis regression in non-diabetic mice, but persist in diabetes and impair regression by exacerbating macrophage inflammation. DNase1 reduced diabetic plaque NETs and macrophage inflammation, and restored atherosclerosis resolution after lipid-lowering, despite ongoing hyperglycemia. Given that humans with diabetes also exhibit impaired atherosclerosis resolution with lipid-lowering, these data suggest that NETs contribute to the increased CVD risk in this population.

2020-05-12 | GSE145200 | GEO

Single-cell genomics reveals a novel cell state during smooth muscle cell phenotypic switching and potential therapeutic targets for atherosclerosis in mouse and human [human]

Project description:Smooth muscle cells (SMC) play significant roles in atherosclerosis via phenotypic switching, a pathological process in which SMC dedifferentiation, migration and transdifferentiation into other cell types. Yet, how SMC contribute to pathophysiology of atherosclerosis remains elusive. To reveal the trajectories of SMC transdifferentiation during atherosclerosis and to identify molecular targets for disease therapy, we combined SMC fate mapping and single-cell RNA sequencing of both mouse and human atherosclerotic plaques.

2020-10-06 | GSE155512 | GEO

Single-cell genomics reveals a novel cell state during smooth muscle cell phenotypic switching and potential therapeutic targets for atherosclerosis in mouse and human [mouse]

2020-10-06 | GSE155513 | GEO

Global effects of 2-methoxyestradiol on smooth muscle cell hyperproliferation and vascular remodeling in atherosclerosis

Project description:We used microarrays to detail transcriptional changes in cultured human smooth muscle cells in response to acute and chronic 2-methoxyestradiol treatment 2-ME, an endogenous metabolite. of estradiol, not only exerts cytotoxic effects on cancer cells but it also protects against multiple proliferative disorders, including atherosclerosis and injury-induced intimal thickening Keywords: treatment vs. control Human aortic smooth muscle cells cultures with/without 2-methoxyestradiol (acute/chronic treatment)

2008-12-30 | E-GEOD-12261 | biostudies-arrayexpress

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